Published
there was a case at a hospital about 4 days ago when a 28 yr old male suffered a massive stroke. there was bleeding in the brain. he was put into a medically induced coma. the next day,he went into full asystolic arrest and after 20 minutes of CPR with no results,the doctor called off the code and patient was pronounced dead. could the stroke itself caused the heart to stop beating?
ST elevated Myocardial Infarct, a classic EKG with a generally unmistakable "elevation" in the ST segment. These patients go to cath lab, STAT- vs a non- stemi, generally medication management.JCD?? Jacob- Creutzfeld (sp.?)
Thank you , and yes :) Have you seen JCD?? I've seen 2 for sure, and 1 questionable- back in 1986-1988...before the whole mad cow thing. It's horrible.
The first one I saw died (of course- only end for JCD). The funeral home comes to pick her up at the hospital and asks us nurses what he's supposed to do with the bodily fluids... Say WHAT? (this was at the beginning of the HIV/bodily fluid precautions) He says he always empties the remains of embalming (body fluids) into the drain, which goes to the regular sewer....great. I live next to this funeral home- and my apt has a pool...no more swimming for this bird....don't care if it's processed at the waste water plant....
ewwww. Evidently, that's what was (don't know what they do now) the norm...The other nurse and I were all 'heebie-jeebies' for the rest of the shift. :grn:
There's not much detail in this case to make a theoretical assumption regarding the physiology that led to the cardiac arrest.We know that this patient had a stroke secondary to a bleed in the brain which in itself is a broad term because you didn't specify the location and type of the bleed. Knowing that piece of information will provide insight on what caused the bleed and what focal neuro deficits the patient would exhibit. You also said that the patient is in a medically-induced coma. The only few times a patient with a stroke will need to be placed on IV drip sedation (or medically-induced coma) is if they are having continuous seizures which could compromise the patency of the patient's airway. In that case, they would need to already be intubated and on a ventilator while the sedation is ongoing. Stroke patients who have neuro deficits severe enough that they are unconscious and unable to clear their airway are intubated and on a ventilator. In addition, there are respiratory centers in the brain that can control a patient's breathing (medulla and pons in the brainstem) and obviously any stroke that affects these structures could lead to absence of spontaneous breathing. But all that alludes to respiratory failure, not cardiac arrest.
You said the patient went into asystolic arrest the next day and was unsuccessfully resuscitated after 20 mins of CPR. The brain controls our breathing but the heart's activity is independent of the brain's control. A heartbeat is caused by activity within the heart's own electrical conduction system, thus, it makes me wonder whether this cardiac arrest is a separate entity from the patient's stroke. A few non-intrinsic cardiac conditions can cause absence of the heart's ability to conduct electrical impulses leading to asystole (hypoxia - i.e., patient could have had a mucus plug while intubated, hypovolemia - i.e., patient is massively bleeding internally or externally, acidosis - i.e., kidney failure, potassium derangements, etc). It could be possible that the patient had other causes of the cardiac arrest such as these non-intrinsic cardiac causes. Knowing that he is only 28, you can maybe invoke the possibility of an intrinsic cardiac event such as myocardial ischemia from an Acute MI. Even then, it's not a situation where the stroke actually caused the asystolic event or cardiac arrest.
There is a direct correlation between the brain and the heart and we see this frequently with neuro patient's with high ICP's........see Cushing's reflex.
Large head bleeds can cause brain herniation and brain hernation is almost always fatal........and everything fatal ends up in cardiac arrest.
well, i'm definitely not a cardiac buff - much more into neuro- good to know !!
tako-tsubo syndrome is a dreadful illness (albeit quite rare) that appears under circumstances of exceptional and extreme stress, at times associated with anger. if this is happening to you, you should try to calm yourself down, if at all possible (although most patients recover completely if supported adequately in a hospital). usually present in cardiogenic shock/congestive heart failure.
in severe shock the microcirculation changes dramatically. those changes are mainly due to a "[color=#ff3300]cytokine storm"[color=#6600cc]induced by extremely severe tissue ischemia or, directly, by a pathogen: (1) the endothelium is activated (vasodilates, becomes pro-coagulant, expresses adhesion molecules), (2) monocytes are activated (and discharge numerous cytokines), (3) white blood cells obstruct some capillaries (4) disseminated intra-vascular coagulation and platelet aggregation plug microcirculation as well. along with microvascualr changes that can lead to the sah.
http://www.stagesofshock.com/microvascular/index.html
takotsubo cardiomyopathy, also known as transient apical ballooning syndrome,[color=#0645ad][1] apical ballooning cardiomyopathy,[color=#0645ad][2] stress-induced cardiomyopathy, gebrochenes-herz-syndrom, and simply stress cardiomyopathy, is a type of non-[color=#0645ad]ischemic[color=#0645ad]cardiomyopathy in which there is a sudden temporary weakening of the [color=#0645ad]myocardium (the muscle of the heart). because this weakening can be triggered by emotional stress, such as the death of a loved one, a break-up, or constant anxiety, the condition is also known as broken heart syndrome.[color=#0645ad][3] stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture
http://en.wikipedia.org/wiki/takotsubo_cardiomyopathy
in the op's senario i would lean towards just a plain ole head bleed. etiology is difficult to determine because you would need more information. some of the causes would include av malformations, spontaneous sah, amphetamine arterteritis, and a percentage remain unknown. some are congenital aneurysms and disorders such as marphans symdrome (a debated issue) . http://findarticles.com/p/articles/mi_hb6374/is_1_33/ai_n28835227/
http://www.strokecenter.org/patients/sah.htm
as the swelling increases inside the closed space of the craninum it will follow the path of least resistance and push downward onto the brain stem ceasing vital functions. when the brain swells to this point it cuts off cerebral circulation. negative cerebral blood flow is brain death and vital organ functions cease. the loss of the brain stem usually causes bradycardia to almost immediate asystole.
http://www.umm.edu/ency/article/001421.htm
http://dynamicnursingeducation.com/class.php?class_id=37
http://health.nytimes.com/health/guides/disease/brain-herniation/overview.html
this causes a phenomenom called cushings triad......increased intercranial pressure, hypertension and bradycardia with pulses paradoxis........http://en.wikipedia.org/wiki/intracranial_pressure.
cushing's triad (not to be confused with the cushing reflex) is a sign of increased intracranial pressure. it is the triad of:
1. hypertension (progressively increasing systolic blood pressure)
2. bradycardia
3. widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time)
cushing's triad suggests a cerebral hemorrhage in the setting of trauma or an space occupying lesion (e.g. brain tumor) that is growing and a possible impending fatal herniation of the brain. cushing's triad is named after an american neurosurgeon harvey williams cushing (1869-1939).
cushings reflex is the biochemical explanation to the cause of cushings triad
whenever a cushing reflex occurs, there is a high probability that death will occur in the near future (seconds to minutes). as a result, when a cushing reflex is detected, immediate care is needed. since its presence is a good detector of high icp, it is often useful in the medical field, particularly during surgery.[color=#0645ad] during any neurosurgery being performed on the brain, there is always a likelihood that raised intracranial pressure may occur. early recognition of this is crucial to the well being of the patient. although direct measurement of icp is possible, it is not always accurate. in the past, physicians and nurses have relied on hemodynamic changes or bradycardia, the late phase of the reflex, to identify the icp increase. once the initial stage of the cushing reflex (tachycardia combined with hypertension) was discovered, it offered a much more reliable and swift warning sign of high icp.[color=#0645ad] it was found that hypertension and tachycardia occurred 93% of the time when cpp (cerebral perfusion pressure map-icp=cpp) dropped below 15 mmhg due to raised icp. also, the cushing reflex is known to arise only from acute prolonged raises in icp. thus, it can be used as a tool by physicians to differentiate acute and chronic rises in icp.
cushing reflex (also referred to as the vasopressor response, the cushing effect, the cushing reaction, the cushing phenomenon, the cushing response, or cushing's law) is a physiological nervous system response to increased intracranial pressure (icp) that results in cushing's triad of widening pulse pressure, irregular breathing, and a reduction of the heart rate. it is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation. it can also be seen after the intravenous administration of epinephrine and similar drugs. (http://en.wikipedia.org/wiki/cushing_reflex)
just my :twocents:..........:)
vanburbian
228 Posts
ST elevated Myocardial Infarct, a classic EKG with a generally unmistakable "elevation" in the ST segment. These patients go to cath lab, STAT- vs a non- stemi, generally medication management.
JCD?? Jacob- Creutzfeld (sp.?)