The Curious Case of the BRAIN and the OCTOPUS trap
There is a certain mental model we form when we hear "brain bleed." This model is formed from previous experience and can lead to lightning speed decisions and intervention. Occasionally, our mental model is disrupted, we stall, and try to link the presentation to something else we have seen. Sometimes this works and other times it can be deleterious. I hope to update your prior model with this story.
Flight Crew Dispatched: Springfield Hospital for 78-year-old female diagnosed with Intracranial Hemorrhage.
Arrival: Patient diagnosed with a significant Subarachnoid Hemorrhage without associated trauma.
Resp: 20- Mechanically Ventilated- nothing fancy
SpO2: 98 % FiO2= 55%
Infusion/Medications: Propofol @ 15 mcg/kg/min for sedation.
Patient packaging was uneventful, and transport was started to the receiving hospital.
In-flight, the patient had a sudden decrease in blood pressure to 82/40 with no other changes. The repeat blood pressure was so scary…I won’t even show it to you!
The transport crew exclaimed- She MUST be herniating! But a reevaluation of the patient found no changes in pupils- which still remained sluggish at 3mm. There was never a report of the patient being hypertensive, widening pulse pressures or bradycardic. So, no obvious Cushing’s Triad……
- Propofol infusion stopped
- 500 ml fluid bolus (lungs clear)
- After no change after fluid bolus
- Flight Crew decided to use a push dose pressor and start an infusion.
Now time to choose the appropriate push-dose pressor and infusion!!!
Neo-Synephrine, or Epinephrine
The crew chose to administer Neo-Synephrine- we will see if they were right.
The patient received a total of 4 doses of 200 mcg Push Dose Neo-Synephrine with minimal improvement in the patient’s blood pressure!
Due to the short transport, the crew never got to picking or starting a vasopressor infusion.
Upon arrival at the receiving hospital, the receiving MD was made aware of the patient’s acute blood pressure issues in transport. Patient systolic blood pressure still remained in the 80's. The receiving MD made an immediate dash for the unit’s ultrasound machine as if he knew what the issue was…
The crew all stared in suspense at the screen as the MD places the probe on the chest to take a look at the heart.
Suddenly they exclaimed- It’s Takotsubo!!!
The medical crew members look at each other in confusion, while still making it look like they know what the doctor is talking about (as we all do!)
So, what is Takotsubo?
It is a form of cardiomyopathy that is defined by left ventricular dysfunction consisting of the loss or impairment of the apex and mid-ventricle.
Why is it called Takotsubo?
The transient LV dysfunction with a characteristic pattern of apical ballooning resembling an octopus trap.
What causes Takotsubo?
STRESS!!!! In 85% of the cases, Takotsubo is caused by an emotionally or physically stressful event to include a stroke. Sometimes Takotsubo is referred to as broken heart syndrome. Although the basic cause of this condition is unresolved, the frequent association with stress has focused attention on the autonomic nervous system. It has been suggested that when powerful catecholamine’s released in excess, the heart muscle can be damaged.
(Emotional and physical stress)
Neurogenic Stunned Myocardium
Acute heart failure in neurologic events has been known for more than a century, with Shanahan describing neurogenic pulmonary edema in 1908. Later it was discovered that virtually all patients with subarachnoid hemorrhage (SAH) and many patients with other neurologic events have ECG abnormalities. Systolic dysfunction usually develops within the first 2 days after a neurologic event and then recovers. Overall, 10% to 28% of patients with SAH have global or regional LV systolic dysfunction.
How do you treat Takotsubo?
- Monitor the QTc interval and arrhythmia. Stop QT-prolonging medications and replete electrolytes.
Treating the cardiogenic shock is a little trickier! As the treatment of cardiogenic shock associated with Takotsubo differs from other forms of cardiogenic shock. The treatment is broken down into 2 groups- Those WITHOUT LV Outflow Tract obstruction (LVOT) or those WITH LV Outflow Tract obstruction- simply put is there an issue with getting blood out of the left ventricle- YES or NO.
First! Try and Avoid Catecholamines- Epinephrine or Norepinephrine, as the disease process of Takotsubo appears to be linked to an excessive amount of catecholamine.
Those WITHOUT LV Outflow Tract obstruction (LVOT)
Treat with inotropes like Dopamine or Dobutamine which will help with the squeeze of the heart…Pretty simple!
Those WITH LV Outflow Tract obstruction (LOVT)
- MOST will have Left Ventricle Outflow Obstruction
-You REALLY want to avoid inotropes in this situation. Increasing the squeeze may only cause the condition to worsen.
- What you want to do is to slow down the heart rate to allow more time for the blood to exit the obstructed outflow tract of the left ventricle. This is done by using a beta-blocker. I know this seems counter-intuitive to treating someone in cardiogenic shock. But this isn’t your normal cardiogenic shock!
While there needs to be a definitive diagnosis made with an ECHO. Someone who is in shock that is highly suspected of having Takotsubo. You could begin treatment with something short acting like Esmolol which can be taken quickly if the patient worsens.
- If vasopressor support is needed. Neo-Synephrine is the drug of choice over Epinephrine or Norepinephrine since these will give more catecholamines.
Soo smarty pants, what happened with the patient above?
-The receiving hospital started the patient on an Esmolol infusion, and the patient's condition improved over the next few hours. No vasopressor support was needed.
- Repeat echo the day after showed the patient no longer had left ventricle outflow obstruction and the left ventricle no longer resemble a Takotsubo.
How would the crew know that the patient had Takotsubo!!!???
The diagnosis of subarachnoid hemorrhages helps guide your thought toward Takotsubo since it’s seen in patients with Subdural/Subarachnoid Hemorrhages. Ultrasound would have been useful for looking at the heart and the left ventricle. But to have a true diagnosis, an ECHO would have to be performed… I will leave the discussion of POCUS for another blog!
Tyler Christifulli, FP-C
Takutsubo secondary to an intracranial hemorrhage is the ultimate booby trap. As a clinician takes to the bedside of a patient with increased ICP, there is no doubt they understand the consequences of hypotension and further decreased cerebral perfusion pressure (CPP). While the majority of patients with increased ICP will be hypertensive, we can see hypotension as a result of herniation. One may be rightfully motivated to start a levophed/epi infusion to maintain CPP. This article highlights the importance of ultrasound in the presence of shock/hypotension. If cardiac ultrasound reveals apical ballooning of the left ventricle, one should switch to a parasternal long view to answer the question of whether the left ventricular outflow tract is obstructed or not. As mentioned in this article, if LVOTO is noted, catecholamines can lead to a worsening of this obstruction and thus a reduction in cardiac output.
Selvage mentions the crew only utilizing push dose pressor due to the length of transport. This is ultimately not what I would ever do. If a patient needs blood pressure management in the hospital, I will likely mix the infusion at the bedside and start it. Anecdotally I believe a clinician is likely to give more pressor when giving push doses as to an infusion. In the end, catecholamines were contraindicated and the diagnosis was made at the receiving facility with ultrasound.
My main take-aways from this article:
There are more pathological reasons for hypotension with increased ICP other than herniation.
Utilization of ultrasound early to determine cause of hypotension and rule out Takutubo.
If ultrasound is no available and pressors seem to be making the issue worst, consider Takutsubo with LVOTO.
Advances in Left Ventricular Dysfunction Research and Treatment: 2011 Edition: ScholarlyPaper Q. Ashton Acton, PhD, Q. (2012). Advances in Left Ventricular Dysfunction Research and Treatment: 2011 (ScholarlyPaper ed.).
Advances in Left Ventricular Dysfunction Research and Treatment: 2012 Edition: ScholarlyPaper Q. Ashton Acton, PhD, Q. (2012). Advances in Left Ventricular Dysfunction Research and Treatment: 2011 (ScholarlyPaper ed.).
“Emotional and Physical Stress.” www.oatext.com, www.oatext.com/takotsubo-cardiomyopathy a-review-of-literature-on-clinical-status-and-meta-analysis-of-diagnosis-and-medical-therapy.php#gsc.tab=0.
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Layon, A. (2013). Textbook of Neurointensive care (2nd ed.).
Neurogenic Stunned Myocardium and Takotsubo Cardiomyopathy Are the Same Syndrome: A Pooled Analysis.(n.d.). Retrieved December 1, 2015, from http://onlinelibrary.wiley.com/doi/10.1111/j.1751-7133.2011.00210.x/full
Takotsubo cardiomyopathy (broken-heart syndrome). (n.d.). Retrieved November 30, 2015, from http://
Takotsubo (Stress) Cardiomyopathy. (n.d.). Retrieved November 14, 2015, from