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Physiological Monitoring of Stroke in the Intensive Care Setting
Physiological monitoring is the cornerstone of critical care; it allows for identifying hemodynamic instability and assessing response to therapy. Utility of most hemodynamic monitoring remains unproven and rather serves as a trigger for detection of cardiorespiratory instability. Some have argued that utility can only be proven if linked to a treatment protocol improving outcome . Noninvasive physiological monitoring includes electrocardiogram (ECG), pulse oximetry, and arterial blood pressure measurement. Invasive monitoring includes arterial catheterization, central venous catheterization, pulmonary artery catheterization, intracranial pressure (ICP) monitoring, and esophageal Doppler echocardiography .
Management of acute ischemic stroke has evolved since 1990s with advances in reducing neuronal injury, post-stroke disability, and death. The advent of dedicated stroke units and neuro-intensive care settings has demonstrated a clear benefit with reduction of mortality independent of age, sex, or stroke severity . Close monitoring of various physiological parameters within these stroke units permits early detection of cerebral edema, blood pressure derangements, pyrexia, hyperglycemia, and oxygenation with expedited care, therefore preventing secondary brain injury. Physiological monitoring of stroke in an intensive care setting is therefore crucial for neuroprotection and decreasing dependency and early mortality .
Noninvasive Monitoring
Electrocardiogram
Ischemic stroke, specifically of the insular cortex, has been associated with ECG abnormalities. Due to its diffuse interconnections with subcortical autonomic centers, the limbic system, and thalamus, the insular cortex plays a crucial role in autonomic function . Insular infarction and its associated laterality can therefore result in autonomic derangements, specifically cardiac arrhythmias. Insular involvement is reported to be independently associated with heart rate (≤64 beats/min), abnormal repolarization, atrial fibrillation (AF), and ventricular and supraventricular ectopic beats . Right insular involvement has been found to result in ECG abnormalities associated with poor prognosis. When adjusted for age, sex, cardiovascular history, and handicap at admission, as well as lesion side, prolonged QTc interval and left bundle branch block were independent predictors of all-cause and vascular mortality at 2 years in right insular infarctions . Right insular lesions are also significantly associated with 2-year all-cause (hazard ratio, 2.11; 95% confidence interval, 1.27–3.52) and vascular (hazard ratio, 2.00; 95% confidence interval, 1.00–3.93) death when adjusted for age, sex, cardiovascular history, and handicap at admission . Insular involvement or elevated high-sensitivity cardiac troponin-T are also associated with a higher risk of paroxysmal AF . These markers as well as older age (median age of 73 years), history of hypertension, and longer duration of ECG monitoring (3 days) increase the detection rate of unknown AF and may warrant a longer duration of ECG monitoring . Acute insular infarction, rather than atherosclerosis at the carotid bifurcation and aortic arch, also contributes to impaired baroreceptor reflex sensitivity. The left insula predominates in causing baroreflex derangements, presumed to be secondary to parasympathetic outflow modulation .
Oximetry
Pulse oximetry is one of the most common modalities used for monitoring in the critical care setting. Continuous oximetry monitoring is required in patients with ischemic or hemorrhagic strokes in order to prevent secondary brain injury due to hypoxemia. This subset of patients is at risk of hypoxemia due to aspiration, hypoventilation, Cheyne–Stokes respiration, atelectasis, or pulmonary embolism . Oxygen content of the brain depends on cerebral blood flow (CBF) and arterial oxygen content. If CBF falls below 10 mL/100 g/min, irreversible damage occurs due to lactic acid production, adenosine triphosphate (ATP) depletion, glutamate release, and sodium and calcium entry into cells progressing to cytotoxic edema and mitochondrial death . Hypoxia also results in anaerobic metabolism, further worsening brain injury . Continuous oximetry targeting safe and acceptable oxygen content is therefore a parameter that can improve outcome in stroke patients. Targeting oxygen saturation >95% has been suggested for patients with stroke . Use of supplemental oxygen for nonhypoxic patients remains controversial. Hyperoxia has been associated with cerebral vasoconstriction and reduced flow, free radical formation during reperfusion, and increased mortality .
Pulse oximeters have many limitations including insensitivity in detecting hypoxemia in patients with elevated baseline levels of P a O 2 or in the presence of carboxyhemoglobin or methemoglobin . Intravenous dyes like methylene blue and blue, green, or black nail polish can cause falsely low S p O 2 levels, whereas falsely elevated levels can be seen with fluorescent and xenon surgical lamps . Motion artifact by far creates the most significant number of falsely low S p O 2 readings. Motion causes equal absorption of both wavelengths resulting in a saturation of 85% . Low perfusion states during systolic heart failure, vasoconstriction, or hypothermia also creates inaccuracy in S p O 2 readings as the oximeter sensor is unable to detect a true signal .
End-Tidal CO 2 Monitoring
Although initially used for anesthesia monitoring, capnography is now used to confirm airway patency and lung ventilation in the critical care setting, field resuscitation, conscious sedation, and emergency medicine. It can be very useful in patients with large hemispheric strokes who are intubated or nonintubated. A change in end-tidal CO 2 (etCO 2 ) reflects a range of pathophysiological states. An increase in etCO 2 can be associated with sepsis, malignant hyperthermia, decreased ventilation, carbon monoxide poisoning, return of circulation following cardiac arrest, and chronic obstructive pulmonary disease . A drop in etCO 2 indicates pulmonary embolus, cardiac arrest, hypothermia, hypometabolic state, low cardiac output, esophageal intubation, and a disconnected ventilator . Capnometry measures fractionated CO 2 (FCO 2 ) in tidal gas at the airway opening using infrared absorption or mass spectrometry. Capnography graphically displays FCO 2 versus time . The two main capnometers used in clinical practice are side stream or mainstream. Mainstream capnometers are comprised of an airway adaptor cuvette attached inline to the endotracheal tube in which infrared light source and sensor detect CO 2 absorption and measure PCO 2 . Mainstream analysis is rapid though limited in nonintubated patients. With a side stream capnometer, a sampling line attaches to a T-piece adaptor at the airway opening for nonintubated patients where it analyzes CO 2 .
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