Covid19 - clinical / epidemiological thread

[deleted171991]

Would you not start an inotrope then? Most trials show no change in mortality but we do it anyways. Just curious how u would manage.

Norepi and more norepi. Would try epi or dobutamine, but only as a second-line agent. Otherwise, I'll probably get tachycardia before significant increase in CO/BP.

In my limited experience, I have noticed that HF patients tend to die from myocardial ischemia due to prolonged and excessive tachycardia due to inotropes. Hence I try to maintain coronary perfusion without increasing the double/triple product. The studies I know about show that even non-infectious acute decompensated CHF patients do better with levo than with inotropes.

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[Arch Guillotti]

Inotropes have been proven not to improve survival, unlike what Manny Rivers wanted us to believe.

Do you start patients on inotropes in the ICU?

 

[deleted171991]

Do you start patients on inotropes in the ICU?

Rarely. But I don't deal with cardiac patients (not that I would in them, either).

I only use inotropes once I have fixed the SVR, if the CO is still low (norepi is also a positive inotrope, being a beta1-agonist, too).

 

[dchz]

In my limited experience, I have noticed that HF patients tend to die from myocardial ischemia due to tachycardia. Hence I try to maintain coronary perfusion without increasing the double/triple product.

This is not a chronic HF patient with poor coronaries. This is a patient population with normal coronaries and normal EF and sudden heart failure sypmtoms. You treat the symptoms and give the underlying path time to heal.

 

[deleted171991]

This is not a chronic HF patient with poor coronaries. This is a patient population with normal coronaries and normal EF and sudden heart failure sypmtoms. You treat the symptoms and give the underlying path time to heal.

If they have sudden heart failure symptoms, their heart is f-ed up. Whether it's the coronaries or inflammation, those myocytes are fighting for survival, with low functional reserve. Not the time to squeeze them. Therapeutic trials tend to support my minimalist attitude. You will rather see me diurese these patients under levophed infusion (if there is fluid overload) than giving them more than a touch of inotropes, if I must (let the heart rest and recover). I will also give epi rather than dobutamine (why give a synthetic catecholamine when I have a "non-GMO" one?).

Possibly due to the fact that I was trained in a MICU where septic patients regularly died while on a ton of infusions (I have also seen a 50 year-old dead after days of tachycardia on dobutamine), I have learned to think twice before doing something, and changing my mind frequently (depending on the results of my therapeutic trials). Still I religiously avoid prolonged tachycardia in my patients, which is usually what one would get from an inodilator without using a vasoconstrictor first.

@dchz and @Arch Guillotti: To be honest, I don't treat enough septic cardiomyopathy nowadays to base your standards of care on my opinion.

 

[marr65]

COVID-19’s mortality spikes in patients aged over 50: report

The fatality rate of the new coronavirus (COVID-19) increased with age, and Korean patients aged over 50 had six times higher mortality than those aged under 50, a medical journal reported. The report particularly noted that the proportion of children and adolescents aged under 19 rose to...

m.koreabiomed.com

Interesting read so far why death rate of Covid 19 in Korea is low relative to other nations. Amazingly, 69% of the infected are from a Christian sect and they are young. If you are 50 and older, better wear that N95 mask all the time and wash hands like crazy. I don’t think this will translate to USA though, the only place would probably be Colorado since they have less obesity and probably less DM,CAD and smoking too. Good luck to the rest of the USA if they are still thinking it’s just the flu.

 

[dchz]

Zoom out to the big picture here, these are young healthy people with no comorbidities. They have sudden decrease in EF.

If they have sudden heart failure symptoms, their heart is f-ed up. Whether it's the coronaries or inflammation, those myocytes are fighting for survival, with low functional reserve.

You can anthropomorphize then all you want, but the fact is the heart is very well understood and it only need ions, oxygen, and good myocytes to run.
They should still have ample oxygen given healthy coronaries, and their myocytes don't just died all of a sudden. So they either

1. went so much to the right side of the frank starling curve and now their healthy myocytes can no longer contract. (the amount of volume that would do this to a healthy person with a previously healthy heart and healthy kidneys is very very high, it makes this almost unlikely).
2. they shifted their frank starling curve to the left/down by having ion problems 2/2 cytokines and other things make the ions channels work incorrectly and causing an ion problem.

The fixing of these ion problems would involve inotropes and the ions.

Possibly due to the fact that I was trained in a MICU where septic patients regularly died while on a ton of infusions (I have also seen a 50 year-old dead after days of tachycardia on dobutamine), I have learned to think twice before doing something, and changing my mind frequently (depending on the results of my therapeutic trials). Still I religiously avoid prolonged tachycardia in my patients, which is usually what one would get from an inodilator without using a vasoconstrictor first.

It's good that your ultimate goal is to have a good outcome for the patient. I am not advocating to make the patient tachycardic indefinitely. The problem is we have low EF most likely due to ions. We fix it by giving it more EF and more ions. If the pt is tachy with good EF now, down titrate the inotrope. Titrating medication to support hemodynamics is literally the crux of our specialty, we can't let the patient down by NOT doing that because of some lousy ICU literature. I would argue those pts in your past died from lack of effective and timely titration of medication rather than the medication themselves.

@dchz and @Arch Guillotti: To be honest, I don't treat enough septic cardiomyopathy nowadays to base your standards of care on my opinion.

Dude i'm just some rando on the internet. But that's beauty of science! you don't need credibility to be right because science is objective.

I don't even need a MD to say: patient has a contractility problem. I will give the patient more contractility.

 

[vector2]

and their myocytes don't just died all of a sudden.

This is exactly what happens in acute, fulminant viral myocarditis. Cytokines play a role in the development of DCM following the infection.
—

Direct viral injury — Our understanding of the pathogenesis of viral myocarditis comes almost entirely from experimental models of acute coxsackie B virus infection [75]. The initial change is myocyte damage in the absence of a cellular immune response. The myocyte injury may be mediated through direct viral toxicity, perforin-mediated cell lysis, and cytokine expression [76].

Intracellular events — Viral entry into the myocyte is mediated by cell surface receptors. The coxsackie-adenovirus receptor (CAR) is a common receptor for coxsackievirus type B and for adenovirus subgroups A, C, D, E, and F [77-79]. The CAR gene has been localized to chromosome 21q11.2 [80]. With rare exceptions, CAR expression is required for virus entry into cells. Observations have established the role for a dominant negative C terminal dystrophin fragment in viral cardiomyopathy and added a new pathway and potential therapeutic target in viral myocarditis [81].

The discovery of the CAR receptor raises the possibility of interventional therapy to block CAR in severe cases of coxsackie B virus or adenoviral myocarditis. Coreceptors, including decay-accelerating factor (DAF, CD55) for some coxsackie B virus strains [82] and integrins, help determine the efficiency of infection [83,84]. The activity of signaling pathways in cardiac myocytes also may determine susceptibility to coxsackie B myocarditis via effects on viral replication [85].

After entry into the cell through the CAR receptor, the coxsackie B viral genome is translated into structural capsid proteins and several proteases that cleave the viral polyprotein. Viral protease 2A can also cleave certain host proteins, and one mechanism of ongoing myocyte injury is through direct interaction of viral proteins with the cytoskeleton. In a transgenic mouse model, cardiac-restricted expression of protease 2A was sufficient to induce dilated cardiomyopathy [86].

Protease 2A cleaves dystrophin in vivo, leading to disruption of the dystrophin-glycoprotein complex that is essential for normal cardiac function [87]. Disruption of the dystrophin-glycoprotein complex is also present in hereditary cardiomyopathies that are related to a dystrophin mutation, such as Duchenne muscular dystrophy [88] (see "Duchenne and Becker muscular dystrophy: Clinical features and diagnosis"). There is more efficient release of the coxsackie B virus from dystrophin-deficient cells [89]. Thus, dystrophin-deficient mice have greater viral replication and more severe cardiomyopathy.
—

UpToDate

www.uptodate.com

 

[vector2]

But more generally it’s a pretty dumb back and forth y’all are having. Suspect decompensated CHF and MAP is low? Rule out ischemia and start levophed, positive pressure, diuretics. Does the pt have improved signs of perfusion vis a vis UOP, warm extremities, normalizing lactate, scvo2, lung water? Great, continue treatment.

But, Pt continues to have cold clammy shock and other bad supportive signs? Now you are at a decision point. If the cause is quickly reversible then a short course of inotropes is fine. You are not fixing the underlying condition but you are making sure the body is getting the oxygen delivery it needs. The problem with decompensated viral myocarditis is that the underlying condition might get much worse really quick. In that case escalating to mechanical circulatory support is the way to go because you rest the heart instead of flogging it.

 

[nimbus]

This is exactly what happens in acute, fulminant viral myocarditis. Cytokines play a role in the development of DCM following the infection.
—

Direct viral injury — Our understanding of the pathogenesis of viral myocarditis comes almost entirely from experimental models of acute coxsackie B virus infection [75]. The initial change is myocyte damage in the absence of a cellular immune response. The myocyte injury may be mediated through direct viral toxicity, perforin-mediated cell lysis, and cytokine expression [76].

Intracellular events — Viral entry into the myocyte is mediated by cell surface receptors. The coxsackie-adenovirus receptor (CAR) is a common receptor for coxsackievirus type B and for adenovirus subgroups A, C, D, E, and F [77-79]. The CAR gene has been localized to chromosome 21q11.2 [80]. With rare exceptions, CAR expression is required for virus entry into cells. Observations have established the role for a dominant negative C terminal dystrophin fragment in viral cardiomyopathy and added a new pathway and potential therapeutic target in viral myocarditis [81].

The discovery of the CAR receptor raises the possibility of interventional therapy to block CAR in severe cases of coxsackie B virus or adenoviral myocarditis. Coreceptors, including decay-accelerating factor (DAF, CD55) for some coxsackie B virus strains [82] and integrins, help determine the efficiency of infection [83,84]. The activity of signaling pathways in cardiac myocytes also may determine susceptibility to coxsackie B myocarditis via effects on viral replication [85].

After entry into the cell through the CAR receptor, the coxsackie B viral genome is translated into structural capsid proteins and several proteases that cleave the viral polyprotein. Viral protease 2A can also cleave certain host proteins, and one mechanism of ongoing myocyte injury is through direct interaction of viral proteins with the cytoskeleton. In a transgenic mouse model, cardiac-restricted expression of protease 2A was sufficient to induce dilated cardiomyopathy [86].

Protease 2A cleaves dystrophin in vivo, leading to disruption of the dystrophin-glycoprotein complex that is essential for normal cardiac function [87]. Disruption of the dystrophin-glycoprotein complex is also present in hereditary cardiomyopathies that are related to a dystrophin mutation, such as Duchenne muscular dystrophy [88] (see "Duchenne and Becker muscular dystrophy: Clinical features and diagnosis"). There is more efficient release of the coxsackie B virus from dystrophin-deficient cells [89]. Thus, dystrophin-deficient mice have greater viral replication and more severe cardiomyopathy.
—

UpToDate

www.uptodate.com

The part that doesn’t make sense is that dead myocytes should release troponin but the description says there is not a rise in troponin.

 

[deleted171991]

The part that doesn’t make sense is that dead myocytes should release troponin but the description says there is not a rise in troponin.

I doubt they are dead. More like hibernating. Septic cardiomyopathy resolves in a couple of weeks. I would expect the same with Covid. Very few viruses give a lethal myocarditis.

 

[dchz]

This is exactly what happens in acute, fulminant viral myocarditis. Cytokines play a role in the development of DCM following the infection.
—

Direct viral injury — Our understanding of the pathogenesis of viral myocarditis comes almost entirely from experimental models of acute coxsackie B virus infection [75]. The initial change is myocyte damage in the absence of a cellular immune response. The myocyte injury may be mediated through direct viral toxicity, perforin-mediated cell lysis, and cytokine expression [76].

Intracellular events — Viral entry into the myocyte is mediated by cell surface receptors. The coxsackie-adenovirus receptor (CAR) is a common receptor for coxsackievirus type B and for adenovirus subgroups A, C, D, E, and F [77-79]. The CAR gene has been localized to chromosome 21q11.2 [80]. With rare exceptions, CAR expression is required for virus entry into cells. Observations have established the role for a dominant negative C terminal dystrophin fragment in viral cardiomyopathy and added a new pathway and potential therapeutic target in viral myocarditis [81].

The discovery of the CAR receptor raises the possibility of interventional therapy to block CAR in severe cases of coxsackie B virus or adenoviral myocarditis. Coreceptors, including decay-accelerating factor (DAF, CD55) for some coxsackie B virus strains [82] and integrins, help determine the efficiency of infection [83,84]. The activity of signaling pathways in cardiac myocytes also may determine susceptibility to coxsackie B myocarditis via effects on viral replication [85].

After entry into the cell through the CAR receptor, the coxsackie B viral genome is translated into structural capsid proteins and several proteases that cleave the viral polyprotein. Viral protease 2A can also cleave certain host proteins, and one mechanism of ongoing myocyte injury is through direct interaction of viral proteins with the cytoskeleton. In a transgenic mouse model, cardiac-restricted expression of protease 2A was sufficient to induce dilated cardiomyopathy [86].

Protease 2A cleaves dystrophin in vivo, leading to disruption of the dystrophin-glycoprotein complex that is essential for normal cardiac function [87]. Disruption of the dystrophin-glycoprotein complex is also present in hereditary cardiomyopathies that are related to a dystrophin mutation, such as Duchenne muscular dystrophy [88] (see "Duchenne and Becker muscular dystrophy: Clinical features and diagnosis"). There is more efficient release of the coxsackie B virus from dystrophin-deficient cells [89]. Thus, dystrophin-deficient mice have greater viral replication and more severe cardiomyopathy.
—

UpToDate

www.uptodate.com

I was gonna make the point about troponins, but @nimbus made it for me.

 

[vector2]

The part that doesn’t make sense is that dead myocytes should release troponin but the description says there is not a rise in troponin.

I don’t know bout COVID but troponin is usually elevated in bad viral myocarditis. Negative troponin does not rule out myocarditis, though.

 

[MoMoGesiologist]

VA ECMO seems a good option for the young as bridge time recovery or transplant

 

[calvnandhobbs68]

not disagreeing, but why would the pulmonary effects be so pronounced and then almost completely resolved before any hint of cardiac abnormality? With a virus those sort of effects are usually simultaneous.

I feel like that's not too wild. If anything the timeline between the two is a bit too short. Typically (at least in kids) we'd see them come back in crumping a week or two after their URI/resp symptoms resolved.

 

[calvnandhobbs68]

I doubt they are dead. More like hibernating. Septic cardiomyopathy resolves in a couple of weeks. I would expect the same with Covid. Very few viruses give a lethal myocarditis.

Eh I mean viruses will give you viral myocarditis-> dilated cardiomyopathy-> pretty lethal for the patient.

And viral myocarditis does give you a bump in troponin. Negative troponin doesn't rule it out but it is seen pretty frequently.

 

[deleted171991]

Eh I mean viruses will give you viral myocarditis-> dilated cardiomyopathy-> pretty lethal for the patient.

And viral myocarditis does give you a bump in troponin. Negative troponin doesn't rule it out but it is seen pretty frequently.

Dilated cardiomyopathy from viral myocarditis is rare in adults. The majority of patients with EKG changes only (due to inflammation) tend to have a self-limited course. Same goes for acute myopericarditis, with preserved LVEF, even with elevated troponins.

It's usually the patients with post-viral or lymphocytic myocarditis who have HF and dilated cardiomyopathy. (Interestingly, the latter have an autoimmune component.) The subtle signs of cardiac involvement can be overshadowed by the systemic manifestations of viral infection.

"Viral injury and post-viral autoimmune response may be simplified into a three-phase model to characterize the stages of the progression of acute viral infection to dilated cardiomyopathy (DCM); the acute viral myocarditis and autoimmune models of myocarditis/DCM development are depicted in the figure (figure 1). The two models do not exclude each other, and may account for the progression from myocarditis to DCM in distinct patient subsets [139].

•The first phase is comprised of viral infection with myocyte death within hours of viral cell entry. In this acute stage, myocyte death results from direct viral damage to myocytes and leads to exposure of host proteins to the immune system.​

•The second phase, which rapidly follows, is an innate immune response comprised of altered regulatory T cell function, natural killer (NK) cells, interferon gamma, and nitric oxide.​

•In the third phase, a virus-specific immune response includes antibodies to pathogen. Non-genetically susceptible animals and humans recover with few consequences. In genetically susceptible experimental animals and humans, a breakdown of T cell tolerance to self-myocardial autoantigens (eg, cardiac myosin) ensues. This leads to chronic myocardial inflammation, necrosis/apoptosis, and fibrosis mediated by humoral (autoantibody-mediated) and/or cell-mediated organ-specific autoimmunity. These patients may die from arrhythmias or progress onto a phase of DCM with chronic heart failure."​

(Source: Uptodate)

So we may be seeing a form of post-viral myocarditis, probably autoimmune rather than a direct viral effect. That would explain why the Covid patients' lungs get better before the heart fails.

 

[Perrotfish]

Does anyone yet know if you can get coronavirus twice? I saw that there are at least two identifiable strains, but has anyone managed to catch both strains? Also has anyone caught the same strain twice or does it reliably produce immunity in those who have recovered?

Its amazing how little actual information I am getting considering how many hospitals are dealing with this. Its all facebook posts and MSN articles. Journals just aren't moving fast enough here.

 

[deleted59964]

VA ECMO seems a good option for the young as bridge time recovery or transplant

how many patients can you put on ECMO?

 

[nimbus]

https://www.google.com/amp/s/www.cbc.ca/amp/1.5491013

 

[dhb]

630 deaths in Italy is that a big bomb in an open area or a small one in a confined space?

 

[Ezekiel2517]

630 deaths in Italy is that a big bomb in an open area or a small one in a confined space?

At least 200 patients in Italy have died in the past 24 hours. They literally have no more ICU beds or vents, their systems are overwhelmed, and their medical infrastructure has collapsed. And they’ve also had thousands of new cases in the past 24 hours.

 

[pjl]

So no source then

“Personal brain” Is probably the best source I have seen cited. Nice enough response I don’t care if it is right or wrong.

 

[propadope]

Management of COVID-19 patients admitted to stepdown or ICU

CONTENTS Rapid Reference 🚀 Initial tests to guide management Chest CT findings Organ support Cardiovascular Respiratory Noninvasive respiratory support Invasive mechanical ventilation Infectious disease – antibiotics Renal Hematology Neurology Immunomodulation Steroid Tocilizumab Baricitinib...

emcrit.org

This is a good read if no one has seen it yet

 

[dhb]

At least 200 patients in Italy have died in the past 24 hours. They literally have no more ICU beds or vents, their systems are overwhelmed, and their medical infrastructure has collapsed. And they’ve also had thousands of new cases in the past 24 hours.

To an individual that has to deal with dying patients in hopital hallways the situation must seem desperate; on an epidemiological level it's not very severe...

 

[Iso4ane]

To an individual that has to deal with dying patients in hopital hallways the situation must seem desperate; on an epidemiological level it's not very severe...

It’s seems more akin mass casualty than a traditional epidemigocal event.

 

[dhb]

It’s seems more akin mass casualty than a traditional epidemigocal event.

Depends on your definition: less than 5k deaths for the moment having already spread to very populated areas

 

[PTPoeny]

To an individual that has to deal with dying patients in hopital hallways the situation must seem desperate; on an epidemiological level it's not very severe...

But as South Korea had shown us many of those deaths could have been prevented. Should we not work to prevent unnecessary deaths?

Proactive quarantine slowed the rate of cases. Even if exactly the same total number of people get sick, fewer will die if there are enough vents. Can you imagine the public backlash as vents are rationed to those most likely to survive here in the US? I have a feeling somehow doctors will be blamed and not the politicians that failed to act that could have prevented the situation with timely action.

 

[Mman]

But as South Korea had shown us many of those deaths could have been prevented. Should we not work to prevent unnecessary deaths?

Proactive quarantine slowed the rate of cases. Even if exactly the same total number of people get sick, fewer will die if there are enough vents. Can you imagine the public backlash as vents are rationed to those most likely to survive here in the US? I have a feeling somehow doctors will be blamed and not the politicians that failed to act that could have prevented the situation with timely action.

public backlash? I can't even fathom the lawsuits it would generate.

 

[anbuitachi]

But as South Korea had shown us many of those deaths could have been prevented. Should we not work to prevent unnecessary deaths?

Proactive quarantine slowed the rate of cases. Even if exactly the same total number of people get sick, fewer will die if there are enough vents. Can you imagine the public backlash as vents are rationed to those most likely to survive here in the US? I have a feeling somehow doctors will be blamed and not the politicians that failed to act that could have prevented the situation with timely action.

probably too early to celebrate. SK cases are rising again, 50 cases a few days ago, now 300+ daily.

 

[deleted162650]

Is there any updated demographic info out of Italy? Still mostly the old/comorbid that are ending up vented/dead??

 

[calvnandhobbs68]

Is there any updated demographic info out of Italy? Still mostly the old/comorbid that are ending up vented/dead??

probably not vented anymore...just dead

The Extraordinary Decisions Facing Italian Doctors

There are now simply too many patients for each one of them to receive adequate care.

www.theatlantic.com

 

[pgg]

But as South Korea had shown us many of those deaths could have been prevented. Should we not work to prevent unnecessary deaths?

Proactive quarantine slowed the rate of cases. Even if exactly the same total number of people get sick, fewer will die if there are enough vents. Can you imagine the public backlash as vents are rationed to those most likely to survive here in the US? I have a feeling somehow doctors will be blamed and not the politicians that failed to act that could have prevented the situation with timely action.

I don't know that South Korea has "shown" us anything.

Their relatively low mortality rate may simply be a reflection of how they tested far more people with mild or even no symptoms.

And Italy's higher mortality rate may simply be an artifact of how they have tested very few people with mild or no symptoms.

We just don't know.

Demographically speaking, Italy is also a pretty old country, and it seems that just about everybody here smokes. Especially the older generations ... even if they aren't current smokers, odds are good that they were chimneys much of their lives. I worry about how much worse Italy is going to get. The epicenter of their outbreak is a wealthier region in the north (Milan, Venice, Florence), but a lot of the south and practically all of Sicily looks like some of the more run-down parts of Detroit, except more rural.

It's a first world country ... technically, according to the original definition.

 

[sevoflurane]

Italy’s mortality rate is a reflection of their disproportionate elderly population

 

[nimbus]

Many of the early Korean patients were young members of the Shincheonji church. Even the Koreans say their mortality rate for patients over 60 is much higher than for those under 60.

Coronavirus death rates in South Korea reinforce a frightening pattern of how the disease affects older people

Death rates in South Korea have been lower than in other countries hit by the coronavirus pandemic, but elderly patients are still more at risk.

www.google.com

 

[sevoflurane]

and they def. like to smoke there still.

Agree with above.

 

[kmurp]

I know one of our larger local hospitals has discussed shutting down the OR for electives if it becomes necessary. For our group, any prolonged 3-4 week shutdown will cause us to be unable to meet payroll as we tend to not have much extra cash on hand this early in the year.

And my hospital just cancelled all electives as of today.

 

[nimbus]

My Updated Plan to Address the Coronavirus Crisis

The actions taken by the Trump administration fall far short of the big public health and economic measures we need to manage the coronavirus.

elizabethwarren.com

 

[deleted171991]

My Updated Plan to Address the Coronavirus Crisis

The actions taken by the Trump administration fall far short of the big public health and economic measures we need to manage the coronavirus.

elizabethwarren.com

More radical socialism (e.g. broad student debt cancellation). So happy she's out.

 

[doctalaughs]

Italian College of Anesthesia, Analgesia, Resuscitation and Intensive Care (SIAARTI) just published guidelines on how to decide who gets critical care and who gets left to die.... that doesn’t bode well.

 

[nimbus]

And my hospital just cancelled all electives as of today.

Region?

 

[Ezekiel2517]

CDC mitigation recommendations for Santa Clara county in the Bay Area include canceling elective and non-urgent procedures. Remember, we’re just at the beginning of this.

https://www.cdc.gov/coronavirus/2019-ncov/downloads/Santa-Clara_Community_Mitigation.pdf

 

[deleted171991]

My Updated Plan to Address the Coronavirus Crisis

The actions taken by the Trump administration fall far short of the big public health and economic measures we need to manage the coronavirus.

elizabethwarren.com

His plan/team is better:

COVID Timeline - Joe Biden for President: Official Campaign Website

In the midst of a growing public health crisis, the country is looking for leadership, effectiveness, and trusted experience — and that’s Vice President Joe Biden. Joe Biden has been laser-focused on the threat that COVID-19 has posed to our nation and the decisive public health and economic...

joebiden.com

 

[kmurp]

Region?

Northeast

 

[agammaglobulin]

I got the same thing here in Seattle.

 

[kmurp]

I got the same thing here in Seattle.

How is your group going to handle the cash flow disruption?

 

[Mman]

How is your group going to handle the cash flow disruption?

you are either not getting paid or you are taking out a short term loan to cover it in the interim.

WTF are hospitals going to do? I mean I can go without a paycheck for a little while, but this can potentially put massive stretch on their resources while simultaneously gutting their cash flow (elective surgeries probably are the only thing keeping most hospitals above water).

 

[kmurp]

you are either not getting paid or you are taking out a short term loan to cover it in the interim.

WTF are hospitals going to do? I mean I can go without a paycheck for a little while, but this can potentially put massive stretch on their resources while simultaneously gutting their cash flow (elective surgeries probably are the only thing keeping most hospitals above water).

We are likely going to have to go the line of credit way by next month. Don't know what we do after that's tapped out. I imagine our CRNAs will want to get paid. Our hospital is already on the edge so that could also be an issue.

 

[hankbb02]

you are either not getting paid or you are taking out a short term loan to cover it in the interim.

WTF are hospitals going to do? I mean I can go without a paycheck for a little while, but this can potentially put massive stretch on their resources while simultaneously gutting their cash flow (elective surgeries probably are the only thing keeping most hospitals above water).

This is a very important issue that isn't being discussed at all. The only solution I see is if the federal government steps in to fiscally support the hospitals.

 

[deleted941485]

This is a very important issue that isn't being discussed at all. The only solution I see is if the federal government steps in to fiscally support the hospitals.

Yeah they’ll support them alright. Medicare reviewers will retrospectively go through the corona cases months later and ask for all the money back.