It’s 2:00 am in the Main ED and you’re racing to get caught up on the board when a nurse comes to notify you about a patient who is still waiting to be seen. A quick glance at the triage chief complaint reads “Cough and fevers x 2 days.” The nurse then hands you the following printout from the vitals machine:
So you do what any good doctor would do. You leap out of your chair like a startled bunny and go to see the patient!
On initial assessment, you find a 67-year-old male who is… A: speaking in full sentences, B: tachypneic and in mild respiratory distress with scattered inspiratory rales bilaterally, and C: diaphoretic, mentating normally, tachycardic and regular. You place the patient on 15L O2 by facemask, move him to a resuscitation bay, and obtain the following ECG:
Regular, wide QRS tachycardia at 150/min
A prior ECG from 2 years ago reveals:
So his ECG today can be further described as an SVT with baseline LBBB.
His bedside lung ultrasound looks something like this:
There are confluent B line artifacts.
His bedside echocardiogram look like this:
Courtesy of pocusatlas.com
There is severely reduced ejection fraction.
Click here for additional case informationHis review of systems is positive for epigastric pain, bilateral arm pain, 2 days of nonproductive cough, 2 days of intermittent diaphoresis, 2 week of bilateral lower extremity swelling. His ROS is negative for fevers, vomiting, bloody, or dark stool.
A chart review reveals a past medical history of HTN, DM, CAD (50% LAD stenosis and 50% LCx stenosis in 2014), cardiomyopathy (EF 35%). He is a former smoker and takes carvedilol, enalapril, HCTZ, glipizide, sitagliptin. He has no known drug allergies.
The secondary survey reveals a diaphoretic male in mild respiratory distress. He has a supple neck with JVD to the angle of the jaw; no anterior cervical lymphadenopathy. He has fine inspiratory rales, no wheezing, regular tachycardia, and no murmurs, rubs, or gallops. His abdomen is soft, nontender and nondistended. He has 1+ bilateral ankle edema. His speech and cognition are normal, cranial nerves are intact; he crosses midline normally and has 5/5 symmetric motor strength.
His portable chest x-ray looks like this:
Labs are significant for:
VBG: 7.34/50/23/24
Lactate: 4.6
Troponin 1.56
Pro-BNP 2719
Based on this these findings, he appears to be in decompensated heart failure with reduced ejection fraction (HFrEF). Differential includes tachydysrhythmia with type 2 MI, pulmonary embolism, and sepsis/pneumonia.
You start the patient on BiPAP, treat him with aspirin 325 mg PO, clopidogrel 600 mg PO, furosemide 40 mg IV, and maybe even a touch of insulin. Cardiology also recommends a heparin infusion in preparation for a left heart catheterization in the morning. The patient’s hypoxemia improves to 92%; however, he remains persistently tachycardic to the 130s and BP falls to 80/40.
You have now entered…
Overview of Cardiogenic Shock
Cardiogenic shock is a syndrome caused by a number of heterogeneous disease entities that all result in end organ hypoperfusion due to primary pump failure. Cardiogenic shock has a mortality between 50-80% and is notoriously difficult to treat. Causes of cardiogenic shock include: (Hochman JS, 1999)
- LV Failure 75%
- Mitral Insufficiency 8%
- Septum Rupture 5%
- RV Failure 4%
- Tamponade 2%
- Other 6%
Common definitions include persistent hypotension (SBP < 90 or a MAP 30 mm Hg lower than baseline) and a cardiac index < 2.0 while on vasopressors and assuming adequate ventricular filling pressures (Reynolds HR, 2008).
The most important equation to remember when managing cardiogenic shock is:
Heart Rate x Stroke Volume = Cardiac Output
Therapeutic Management of Cardiogenic Shock
The goal of medical therapy is to bridge the patient to an intervention that can produce a durable improvement in cardiac output. Bridging to early primary percutaneous coronary intervention (PCI in < 6 h for patients with NSTEMI) or CABG can correct ischemia as the underlying cause for myocardial dysfunction and improves 6-month mortality (Hochman JS, 1999). Patients with chronic LV failure, alternatively, may be bridged to a mechanical support device and ultimately to cardiac transplant in appropriate patients.
The mainstay of medical therapies for cardiogenic shock are inotropes and vasopressors based on their ability to improve cardiac output.
The most important thing to know about pressors in cardiogenic shock is that dopamine may be associated with increased mortality in cardiogenic shock when compared to norepinephrine. De Backer et al (2010) found that patients given dopamine had more clinically significant arrhythmias. Even more importantly, they found a higher overall 28-day mortality in the subgroup of patients with cardiogenic shock who were treated with dopamine. Norepinephrine is well established as first-line vasopressor for septic shock (Dellinger 2013), and mounting evidence shows norepinephrine should be the default pressor for most shock syndromes, including cardiogenic shock (Gamper et al 2016).
Norepinephrine has strong α1, moderate β1, and weak β2 activity.
Beta-adrenergic activity raises the heart rate and has a mild inotropic effect. Alpha adrenergic activity constricts peripheral arterioles, increasing systemic vascular resistance (SVR) which reduces stroke volume. The end result is a small net change in cardiac output, however the alpha stimulation raises blood pressure and shifts blood away from the periphery and toward the coronary arteries and brain.
Inotropes
While routine use of inotropes is not indicated for chronic heart failure, inotropes are essential in resuscitating a patient with end organ hypoperfusion due to cardiogenic shock. In general, inotropes should be utilized at the lowest dose required to achieve clinical effect.
Dobutamine has strong β1, moderate β2, and weak α1 activity.
Greater β activity results in increased HR and SV (and thereby cardiac output) at the cost of increased oxygen demand, which can be harmful in ischemic states. Dobutamine also dilates renal arterioles which is why you may hear it described as “renal protective.” It decreases SVR, however, which can result in a lower blood pressure.
Milrinone is another inotrope that is often used in ICU settings; it’s half life is MUCH longer than dobutamine (almost a full day compared to a few minutes with dobutamine), so it is rarely initiated in the ED. In myocardial cells, milrinone opens Ca channels which improves cardiac inotropy. In smooth muscle, milrinone increases cAMP, which inhibits smooth muscle myosin light chain kinase, leading to both arterial and venous vasodilation. This can lead to profound hypotension and dysrhythmias which can last for as long as the milrinone does. In general, it is recommended only for refractory cardiogenic shock.
Here is a comparison of the hemodynamics of dobutamine vs milrinone:
Adjuvant Therapies
Calcium
It is worth mentioning that calcium chloride or calcium gluconate may improve cardiac inotropy, especially in hypocalcemic patients.
Vasopressin
Vasopressin leads to increased calcium release from the sarcoplasmic reticulum in smooth muscle, leading to vasoconstriction. This is not only a useful synergistic mechanism in combination with norepinephrine, but it can also oppose the hypotension generated by milrinone.
Conclusion
Now that we have had a chance to review the management of cardiogenic shock, we are ready to assist our patient (who remains persistently tachycardic to the 130s and has become hypotensive). For his hypotension, I would recommend that we support his blood pressure with norepinephrine.
Given his bedside echo, he may also require an inotrope. Remember, however, that dobutamine is primarily β1, which will increase his already high heart rate. Perhaps, instead, we should attempt to address his tachycardia. We could give adenosine to assess for an underlying SVT (i.e. diagnostic and perhaps therapeutic). If his tachycardia is atrial flutter or inappropriate sinus tachycardia, then rate control with esmolol may actually help improve ventricular filling and therefore stroke volume as well.
If after rate control and vasopressors the patient remains persistently hypotensive, milrinone could potentially improve his inotropy via a non-adrenergic pathway, although this should be given in small increments – you can’t take it back once you’ve given it. Vasopressin would also be a useful adjunct in this scenario.
Given this patient’s known coronary artery disease, he may really need urgent revascularization, which in the absence of a STEMI on ECG, would mean he needs a CABG.
By Paul Pukurdpol, Kings County EM Resident, PGY-4
References
- Hochman JS, et al. “Early revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock.” NEJM, 1999, 341(9), 625-634.
- Reynolds HR, et al. “Cardiogenic Shock: Current Concepts and Improving Outcomes.” Circulation. 2008;117:686-697.
- De Backer D, et al. “Comparison of dopamine and norepinephrine in the treatment of shock.” NEJM 2010;362(9):779–89.
- Dellinger RP, et al. “Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012.” Critical Care Medicine 2013;41(2):580–637.
- Gamper G, et al. “Vasopressors for hypotensive shock (Review).” Cochrane Database of Systematic Reviews 2016, Issue 2.
- Abraham WT, et al. “In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an Analysis from the Acute Decompensated Heart Failure National Registry (ADHERE).” J Am Coll Cardiol 2005; 46:57–64.
Charles Murchison
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4 Comments
angelagcai · August 2, 2018 at 11:33 am
I’m wondering about the use of furosemide in this case based on Marino’s ICU book chapter on acute heart failure. Marino generally advocates for vasodilators (e.g. nitro) first with the addition of diuretics if cardiac filling pressure (i.e. PAWP) is not adequately reduced or if there is evidence of hypervolemia. His reasoning is that furosemide can decrease cardiac output (via decreased venous return) and increase LV afterload (via vasoconstriction from renin release). In this case, what was the thought process behind giving furosemide instead of or without any vasodilators? Thank you for this well written, educational post.
Ian deSouza · August 3, 2018 at 4:54 pm
Great question. This patient likely had a subacute, supraventricular tachycardia with baseline systolic dysfunction and had developed volume overload and pulmonary edema over time. Here, management of the the tachydysrhythmia (which should improve cardiac output) along with diuresis (to improve oxygenation) would be indicated first. If hypotension ensues, then add vasopressor.
This case is different than the typical APE patient with acute DIASTOLIC dysfunction and severely elevated LV pressure as result of increased after load (ventricular-vascular dysynchrony). This is when you aggressively use BiPAP and vasodilation such as bolus-dose NTG or high-dose infusions.
Viau DM, Sala-Mercado JA, Spranger MD, O’Leary DS, Levy PD. The pathophysiology of hypertensive acute heart failure. Heart 2015;101:1861-7. doi: 10.1136/heartjnl-2015-307461
nino · April 30, 2020 at 5:09 pm
Can we give negative chronotropic drugs to menage high HR due to inotrope itself, to patients on inotropic support?
wchan · May 19, 2020 at 8:10 am
Great question. Inotropes are commonly used in resuscitation on patients with end-organ hypoperfusion. Inotropes can have an effect on both the alpha and beta receptors in the vessels and the heart. In a case like this, with cardiac shock, dobutamine might be required with its beta activity. Dobutamine has β-agonists to increase contractility, which increases overall cardiac output. There are several cases/reports demonstrating the successful use of negative chronotropic drugs (β-antagonist) to manage unwanted side effects of inotropes.
In stress echo exams using dobutamine, low dose esmolol is commonly used to improve imaging acquisition (Abdullah et al, 1997). In addition, it has been reported that concurrent use of the beta-antagonist esmolol helps manage symptoms, such as increased HR, and improve dobutamine-induced diastolic hypotension. However, be aware, there have been rare cases of coronary vasospasms with esmolol administration (Martinez et al, 2015). There have been several animal models (in mice and pigs) that have shown synergetic effects with esmolol and dobutamine, as well as with esmolol and norepinephrine (Muchada et al, 2001).
A small Italy ICU study reported improvement with esmolol infusion in patients with severe septic shock requiring NE (Morelli et al, 2013). The study reported reduced needs for vasopressors and IV fluids, as well as improved hemodynamic parameters. The authors proposed that the addition of beta-antagonists can reduce the toxic effects of catecholamine and improve diastolic fill.
Overall, you can use negative chronotropic drugs while concurrently using pressors for inotropic support; it can improve the side effects of inotropic drugs, but may come with cardiac side effects.
Abdullah, E.E., Pollick, C. Symptomatic and hemodynamic recovery following dobutamine stress echo: benefit of low-dose esmolol administration. Int J Cardiovasc Imaging 13, 53–57 (1997). https://doi.org/10.1023/A:1005710309714
Martinez, AM., Del Riquelme MM, etc. Coronary vasospasm after dobutamine stress
echocardiogram triggered by esmolol. Int J Cardiovasc 193:17-9 (2015). doi:
10.1016/j.ijcard.2015.04.272
Muchada R., etc. Dobutamine and Esmolol, Opposite Action or Sometimes Synergic
Therapeutic Actions. Anaesthesia, Pain, Intensive Care and Emergency Medicine 193:17-9 (2001). 825-834
Morelli A et al. Effect of Heart Rate Control With Esmolol on Hemodynamic and Clinical Outcomes in Patients With Septic Shock: A Randomized Clinical Trial. JAMA 310(16):1683-1691 (2013). doi:10.1001/jama.2013.278477