Although the phrase transient ischemic attacks sound complicated, its meaning is fairly straightforward. A TIA is a temporary interruption in the blood supply to a portion of the brain, which usually doesnt last more than a few minutes or few hours. TIA's can be caused by travelling clots, just as in full fledged stroke, or they can be caused by clogged up artery walls. Infact, the only difference between a TIA and a stroke is that a TIA is temporary. Clots or clogging deposits are eventually broken up or dissolved.
Symptoms: Visual loss, weakness or numbness, slurred speech, loss of speech, vertigo, loss of balance. Before the clot or deposit disappears, symptoms may appear. As with a completed stroke, the symptoms of TIA also depends on the area of brain where the blood supply was interrupted. Unfortunately, because these symptoms disappear, sometimes within minutes, they are often ignored. Furthermore, because they are often vague or mild we often ignore them. After all , who wants to believe that they could be having a stroke? But therein lies the danger of TIA. Yes its symptoms fade, but the underlying mechanisms that created it still are hidden within our bodies. Blood still can be filled with cholesterol. Artery walls can still be vulnerable. Clots still can be forming. For a TIA to be an effective warning, medical intervention is crucial. This is an emergency! Period.
Preventive measures for hypertension, diabetes, high cholesterol or any of the controllable risk factors can be initiated only if a physician is made aware of your TIA symptoms immediately though you may find them inconsequencial. Here are the most common symptoms: Temporary weakness, numbness, or paralysis of the hand, arm, leg or face on one or both sides of the body are the most crucial "red flag" symptoms. and if immediately brought to your physicians atention, can save your life. One note: this weakness or numbness is not the same thing as the pins and needles you feel when , for example your foot falls asleep. It comes quickly and leaves just as fast.
Sudden blurred, dimmed, or complete loss of vision in one or both eyes that lasts longer than a few seconds.
Speech and language difficulties which can involve having trouble actually speaking and understanding the spoken word( aphasia) or the written word (alexia). Slurred or thick speech ( disarthria) can also be presented as symptoms of TIA. Other symptoms may include lack of coordination or balance( ataxia), vertigo, which should be associated with other symptoms, for it to signify an attack. For example dizziness without numbness, weakness, or speech problems is rarely a sign of TIA. Similarly nausea or vomiting in combination with other symptoms of TIA can signal a possible attack. TIA is reversible. Heeding its warning signs can go far in preventing a stroke. But sometmes the "dreaded impossible" occurs, despite our best intentions and care.

Acute coronary syndrome or ACS is an umbrella term used for any condition characterized by symptoms of acute myocardial ischemia caused by an abrupt reduction in blood flow to the heart. Three related but distinct clinical entities fall under the category of ACS; Unstable Angina (UA), Non ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI)
Unsable Angina; This occurs when a thrombus partially or intermittently blocks blood flow through a coronary artery. It is characterized by the development of chest pain that may or may not radiate. The chest pain may be associated with additional symptoms such as dyspnea, diaphoresis, nausea, lightheadedness, elevated heart rate, hypo or hypertension, and arrhythmias. Chest pain occurs with rest or exertion: the pain and associated symptoms are severe enough to limit the patients activity. A 12 lead ECG will show transient / temporary ST- segment depression or T-wave inversion. Cardiac biomarkers are not elevated. Chest pain that occurs with minimal exertion or requires an increasing dose of sublngual nitroglycerine to obtain relief is defined as UA. It also includes prolonged episodes of chest pain at rest, any chest pain that increases in severity, or any chest pain that is very severe upon first presentation.
NSTEMI; Also occurs when a thrombus partially or intermittently blocks blood flow through a coronary artery. On initial presentation, it may be difficult to differentiate between UA and NSTEMI. Like unstable angina, it is characterized by chest pain that may or may not radiate to the arm, neck, back or epigastric region. The chest pain may be accompanied by additional symptoms such as dyspnea, diaphoresis, nausea, lightheadedness, tachycardia, hypo or hypertension, arrhythmia and a drop in oxygen saturation. Pain may occur at rest or with activity. Compared with UA chest pain in NSTEMI lasts longer and is more severe. A 12 lead ECG may show signs indicative of myocardial ischemia.; ST segment depression or T wave inversion. Diagnosis of NSTEMI is made on the basis of elevated cardiac biomarkers.
STEMI; Occurs when a thrombus fully occludes a coronary artery resulting in necrosis of part of the myocardium. Development of an acute MI is characterized by a central necrotic area surrounded by zone of injury. Tissue in the zone of injury can recover if blood flow is restored quickly enough; if it is not, the area of injury will become necrotic. The zone of injury in turn, is surrounded by outer zone of reversible ischemia. Like other forms of ACS, STEMI is characterized by chest pain that may or may not radiate to the arm, neck, back, or epigastric region. Accompanying symptoms may include dyspnea, diaphoresis, nausea, lightheadedness, tachycardia, tachypnea, hypo or hypertension, a drop in oxygen saturation and arrhythmias. Also like UA and NSTEMI, this pain may occur at rest or with exertion and is severe enough to limit the person's activity. Quantitatively, pain is longer in duration and more severe than chest pain in UA. Definitive diagnosis of STEMI is made on the basis of 12 lead ECG changes indicative of MI. Serum biomarkers are elevated.
Adherence to evidence based guidelines for the management of ACS has been associated with better patient outcomes and decreased risk for subsequent cardiac events such as recurrent ischemia/ infarct.

Shivering is a normal physiological response of an individual's sensed temperature and the thermostatic-like response of their threshold zone. Incoming signals of "cold" from the periphery provides the input information to the central control mechanism (hypothalamus) and initiates thermoregulatory responses. When hypothermia develops either accidentally or intentionally induced, the body will immediately try to counteract this disturbance to decrease heat loss by vasoconstriction and piloerection (gooseflesh) followed by shivering, a thermoregulatory mechanism.Febrile shivering is the shaking chill experienced during fever. The observed increase in skeletal muscle activity results in increased heat production until the body temperature reaches the new thermostatic set point.
Temperature reduction therapies have been proven to provide substantial protection against ischemic brain injury and also to slow and prevent brain injury. Induced moderate hypothermia which purposely lowers the body temperature below normal has seen to improve neurological outcome in survivors of cardiac arrest. Traumatic brain injury guidelines recommend mild to moderate hypothermia or normothermia for neuroprotection. But shivering, one of the common side effects seen with therapuetic cooling remains a serious limitation to this therapuetic modality and must be controlled in order to avoid serious physiologic consequences.
A growing body of evidence shows that vigorous shivering can increase metabolic heat production upto 600% above basal level, even in febrile patients. Shivering is not only uncomfortable, it also increases intracranial pressure and has undesirable effect in patients with primary neurological and post hypoxic brain injury. Shivering can double or even triple the oxygen consumption causing hypoxemia, myocardial ischemia in high risk patients because of increased myocardial demand. This has a particularly negative impact on post cardiac arrest patients whose heart has just been resuscitated. Therefore, avoidance of shivering is strongly recommended during hypothermia induction, normothermia or rewarming periods.
Shivering is most likely to occur when the core temperature is 34-36 deg celcius.The ideal goal in shivering management is prevention. Protection of cold sensitive cutaneous receptors from direct cold contact and avoiding skin exposure and contact with cold surfaces and use of warm packs should be the first step to minimize the risk of shivering. In current clinical practice, several sedatives, anaesthetics and opiate drugs and neuromuscular blocking agents are utilized to suppress shivering activities. (in neuro ICU) Many of these agents can compromise airway defense and respiration and they are used for intubated and mechanically ventilated patients only.
Neuroscience nurses often encounter a multitude of challenges managing fevers in their patient population. The efficiency of the cooling modality is critically important since the therapuetic window to implement neuroprotection is very narrow, and " time is brain" The neuro ICU nurse's bedside practice focusses on ease of initiating cooling therapy, the speed of fever reduction, and maintaining tight temperature control. Traditional cooling blankets and even the newer skin surface cooling methods have limited impact on core cooling and also induces shivering which is seen to be detrimental. For patients who need cooling measures specially with neuronal injuries intravascular cooling technology has been shown to be more effective and superior in reduction of visible and subclinical shivering compared to several methods of skin surface cooling and use of antipyretics .It is effective in transferring or removing heat directly within the core thermal compartment via a central venous catheter. This also means less usage of sedatives, neuromuscular blocking agents, opiates etc to prevent shivering thereby promoting better ventilation.
Therefore while considering methods to induce hypothermia and fever control to optimize neurological outcomes, shivering should be anticipated as a normal thermoregulatory response and as far as possible it must be prevented and controlled.