Types of scalability

neuro-genic stunned myocardium.

4. Troponin < 2.8 ng/mL and EF < 40% in the setting of acute aneurysmal SAH is consistent with stunned myocardium rather than a true coronary event.

These tips are only true in general and, as such, care for each patient must be individualized. Nevertheless, it is helpful to remember how to differentiate these two entities in the emergency department in order to prioritize the procedures for managing the patients. Typical stunned myocardium patients should be treated with securing of the ruptured aneurysm in order to avoid rebleed and then providing appro-priate hemodynamic support (avoid the use of pure alpha₁-adrenergic receptor agonist). The use of inotropic agents in order to support the reduced contractility and low EF while paying close attention to keep the patient euvolemic is essential (neglecting to address intravascular volume depletion in the setting of stunned myocardium would require a higher than necessary amount of vasopressors and may cause worsening of the cardiac injuries). Initiating prophylactic triple-H therapy in a patient with neurogenic stunned myocardium during the first few days of SAH may be more harmful than beneficial.

Figure 1-11. Cerebral T wave in neurogenic stunned myocardium syndrome (deep, inverted T waves with pro-longed QTc intervals, so-called “cerebral” T waves are seen in this patient with aneurysmal SAH).

I aVR V1 V4

V5

V6 V2

V3 aVL

aVF II

III

! cRItIcAL conSIDERAtIonS

• Acute aneurysmal A is a dynamic particularly true ith poor grades disease lose neurologic observation and monitoring is required from the beginning and throughout the entire vasospasm precaution period. Just because patients are doing well, that does not nec-essarily mean he/she would continue to do well. Stopping TCD or neurochecks after 7 days for a Fisher group 3 patient who has been doing well is not recommended.

• oor grade A patients have stupor and coma e amination, and therefore the value of the bedside clinical examination is limited. It is a good idea to perform a surveillance CTA and CTP for these patients in the middle of the peak vasospasm period even if examination remains the same.

Figure 1-12. A.Apical ballooning on left ventriculogram, which is similar in shape to a takotsubo (Japanese octopus trap jar), demonstrating apical ballooning. B. Contraction of the heart is normal and hyperdynamic only at the base, and the apex is severely dilated and hypokinetic.

A B

care

• grade is associated ith long term clinical outcome and the isher scale is associated ith risk of symptomatic vasospasm. The modified Fisher scale was developed in order to provide a more practical scale while incorporating the importance of IVH as an independent risk factor for DCI. The IVH alone, however, is not strongly associated with vasospasm, as it is uncommon to see vasospasm in patients with isolated IVH due to hypertension. Using more advanced, automatic outlining software to quantify the hemorrhage volume may provide useful information regarding the exact threshold of the volume in its relationship with the risk of DCI and outcomes.

• t is important to remember that the most consistent predictive variable for is the amount of the hemorrhage.

• hen a patient presents ith high grade A , , and obstructive hydrocephalus ith a large amount of cisternal blood burden (after ABC), the first thing to do is to place a ven-tricular drain, immediately. After placing the drain, it is important to ensure that the drain is working properly (provided that the full medical and surgical intervention is what the patient would want).

• crisis is a ma or challenge in the acute phase typically first ee of poor grade A Aggressive, timely intervention is necessary in order to avoid secondary neuronal injury.

In addition to EVD placement, sedation, hyperventilation, mannitol/hypertonic saline, and pentobarbital have been the conventional therapies. Recently, therapeutic hypothermia has been reported in the literature and may be useful in treating the refractory cases.

• A management is not only about and The brain o ygenation as ell as the brain metabolic distress status may be important targets for successful resuscitation of the high-grade SAH cases.

• oal driven therapy of targeting the hemodynamic variables by optimi ing the delivery as well as the perfusion of oxygen may help by reducing the damage mainly by avoiding sec-ondary injury while giving the brain a chance to recover.

• ymptomatic cerebral vasospasm continues to be a ma or challenge bleed days to are the usual peak period. Ultra-early vasospasm has been reported, but this is less common.

• ctal infarction may occur in A , hich represents the ischemic in ury that occurs at the time of the rupture of an aneurysm rather than due to DCI.

• asospasm may be detected by using a number of different modalities T , TA, T , cEE , and angiography (yes, of course you can and should do a good clinical examination, but under-stand this may be limited for high-grade SAH patients). Obtaining the angiogram quickly is the key, as delays in treatment by either IA vasodilators or balloon angioplasty may lead to irre-versible ischemic damage. From the onset of acute, severe neurologic deficit, IA intervention should not be delayed by more than 2 hours, particularly if full medical support [triple-H] has already been initiated. Symptomatic vasospasm that is refractory to full medical therapy hap-pening in the middle of the night should not and cannot wait until the next morning. This is a medical emergency and stat angioplasty must be done. Triple-H therapy is not an appropriate substitute for an angioplasty. (Yes, it is a good idea to make sure the patient is euvolemic with high blood pressure on board, but that does not mean the angioplasty can happen many hours later in a symptomatic patient just because the patient is being treated with triple-H therapy.)

• A in ection of nicardipine and verapamil papaverine is not commonly used anymore recently milrinone has been used) is useful in treating vasospasm but in some cases the posi-tive effect may not last long. One may argue that such short-lasting IA nicardipine/verapamil is not necessarily consistent with “nicardipine/verapamil failure,” as the therapy did work while the patient was in the angiography suite and the patient did well afterward for several

hours. Regardless of what it is called, the bottom line is that the effort should be focused on minimizing and avoiding the stroke secondary to the vasospasm or recurrence of the vasospasm. If the IA injection of vasodilator therapy was only good for 6 hours, then another therapy of IA injection at that time or balloon angioplasty is needed in order to avoid stroke.

If IA nicardipine or verapamil lasted 6 hours, and patient is symptomatic again, then another therapy is emergently needed at that time, not the next day.

• There is no evidence that opening up a spastic, symptomatic vasospasm leads to higher ris of reperfusion injury and hemorrhage—avoiding angioplasty and IA treatment for acute vasospasm may not be justified based on theoretical fear, as it is clear what the outcomes are when someone is acutely hemiparetic on full triple-H therapy due to severe vasospasm (the patient will most likely not be able to move that arm again if left untreated).

• f you have a three stri e rule ie, vasospasm needs to be treated ith nicardipine or verapamil three times [or twice for a two-strike rule] before any balloon angioplasty can be considered), it is important to remember that every time the patient becomes symptomatic there is a risk of having irreversible ischemic damage.

• or refractory, symptomatic vasospasm, both partial aortic occlusion and intra aortic bal-loon counterpulsation therapy has been shown to improve CBF and reduce neurologic def-icits based on anecdotal reports. Further studies are needed before recommending these therapies as routine treatment.

• and A can have very similar laboratory findings and therefore can be challenging to differentiate. A common therapy for both entities is to replace sodium. Hypertonic saline is a reasonable option for both. For aneurysmal SAH patients who develop symptomatic or significant serum hyponatremia, avoid aggressively promoting free water loss or severe fluid restriction as this may make CSW worse and can potentially be dangerous. IV conivaptan and PO tolvaptan should not be used for hypovolemic hyponatremia due to CSW as this can lead to severe intravascular volume depletion. Having intravascular volume depletion in the setting of symptomatic and angiographic vasospasm is a cocktail for ischemic injury.

• Assessing serum uric acid may be helpful in differentiating versus A after suc-cessfully reversing hyponatremia.

• eurogenic stunned myocardium occurs not uncommonly after A especially ith high grades), and the troponin level may rise significantly.

• hile the E alone cannot differentiate myocardial infarction from stunned myocar-dium, there are a few helpful tips: severely depressed EF with nonspecific, cerebral T waves 10-fold higher troponin values for MI and usually only mildly elevated troponin for stunned myocardium and quick reversibility of stunned myocardium with adequate hemodynamic support by judicious use of pressors and inotropic agents (eg, avoiding increased use of phe-nylephrine while the patient is severely volume depleted and having an EF of 20%: simply using IV Neo-Synephrine [phenylephrine] prophylactically to increase the blood pressure in the absence of symptomatic vasospasm is only going to make cardiac injury worse).

• igh grade A can be a dynamic disease, typically ith multiple phases of challenges first phase, ICP crisis; second phase, vasospasm; third phase, difficulty weaning the ventilator and ventricular drain needing ventriculoperitoneal shunt (VPS); fourth phase, dysautono-mia and sympathetic storming.

• A patient ith grade A can potentially have a decent long term neurologic outcome (modified Rankin score of 1 to 3 is possible) if aggressive medical and surgical care are provided. Premature withdrawal of care may be a self-fulfilling prophecy. While continuing

care medical care may not always lead to good outcomes (and the goals of care should be deter-mined by the patient’s known wishes and what would be the best interest for the patient), patients with HH grade IV and even V may have a chance to recover. Prognosis is not always accurate on high-grade SAH patients during the first few hours or during the first day of a bleed especially prior to performing an EVD placement.

• n patients ith acute early administration of bloc ers reduces the rate of reinfarction and chronic administration improves survival o ever, bloc ers, even ith the ones ith short-acting properties, should not be administered to patients who are hypotensive or with other signs of shock.

• iltia em and verapamil are contraindicated in patients ith TE and associated systolic left ventricular dysfunction and CHF.

• An early invasive strategy coronary angiography ith possible percutaneous transluminal coronary angioplasty) is favored in patients with unstable angina or NSTEMI who have any of the following high-risk indicators: recurrent angina or ischemia despite intensive anti-ischemic therapy; elevated troponin; new or presumably new ST-segment depression; recur-rent angina or ischemia with CHF or new or worsening mitral regurgitation; a high-risk noninvasive stress test; left ventricular ejection fraction less than 40%; hemodynamic insta-bility; sustained ventricular tachycardia; PCI within the last 6 months; and prior coronary artery bypass graft surgery.

• Echocardiography is not useful in diagnosing A in patients ith chest pain o ever, it is essential in diagnosing mechanical complications of acute MI.

• Elevated serum cardiac biomar ers and T segment elevation and or depression can occur in the absence of ACS.

• ost myocardial complications include cardiogenic shoc , , left ventricular free all rupture, ventricular septal rupture, ischemic mitral regurgitation, or papillary muscle rup-ture causing acute mitral regurgitation.

• E findings suggestive of A are often present in patients presenting ith subarach-noid hemorrhage, cerebral infarction, and intracerebral hemorrhage even in the absence of underlying coronary artery disease.

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