Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Region 8 EMSS April 2017 Altered Mental Status / Stroke Objectives • Define altered mental status – Review Causes – Review Corrections – Review Treatment • Define stroke – Review Causes – Review Treatment Introduction • • • • • • Region Updates System Updates SME video of the month Review of altered mental status SOP’s Review of Stroke SOP Scenarios Announcements • Region • System – CDH • Reminder that all patients with a GCS less than 15 require capnography to be used during care. SME video Altered Mental Status Defined • Altered mental status is defined as a change in level of consciousness and cognitive function from normal baseline • Mental status has several components arousal, awareness and cognitive function Altered Mental Status Defined • Arousal: – The level of alertness, spontaneous eye opening, stimulation to wake, inattention • Awareness: – Perception of the environment • Cognitive function: – Includes reasoning, memory, attention and language Altered Mental Status • What may be considered altered level of consciousness? – Patient is not awake – Patient is unaware of their environment – Patient is not oriented to person, place or time – Patient is confused – Patient is unable to comprehend commands – Knowing the baseline mental status of the patient is important in detecting subtle changes in mentation Altered Mental Status Tools • Glasgow Coma Score (GCS) – Using a GCS vs. AVPU will allow EMS providers to more accurately monitor subtle changes in mental status from baseline and during reassessment. Eyes Verbal Motor 4 Opens Spontaneously 5 Alert X 4/4 6 Spontaneous Movement 3 Opens to Voice 4 Confused 5 Localizes Pain 2 Opens to Pain 3 Inappropriate 4 Withdraws From Pain 1 No Opening 2 Incomprehensible Sounds 3 Decorticate Posturing 1 No Verbal Sounds 2 Decerebrate Posturing 1 No Movement Altered Mental Status Tools • Using AVPU will allow providers to obtain a rapid “sick or not sick” assessment, however, subtle changes in mental status may not be noticed if only relying in AVPU. – Alert – Verbal – Painful – Unresponsive Altered Mental Status Tools • AVPU vs. GCS AVPU Alert GCS Ranges 15 Verbal 4-14 Painful 4-10 Unresponsive 3 • Using AVPU alone may not capture acute changes in mental status Altered Mental Status Causes • To ensure proper treatment the EMS provider should attempt to identify the cause of the mental status change. Using the pneumonic AEIOU-TIPS and the H’s and T’s can be useful tools in the initial assessment process if a obvious cause is not easily identified. Altered Mental Status TIPS • • • • • • • • • A E I O U T I P S Alcohol Epilepsy or seizure, endocrine Infection Overdose (opiates) Uremia Trauma, blood loss, shock Insulin Poisoning/psychiatric Stroke, syncope Altered Mental Status H’s and T’s • • • • • • • • • • H H H H H T T T T T Hypovolemia Hypoxia Hydrogen Ion Hypo/Hyperkalemia Hypothermia Tension pneumothorax Tamponade / cardiac Toxins Thrombosis, pulmonary (PE) Thrombosis, cardiac / neuro Altered Mental Status Tools • AEIOU-TIPS vs H’s and T’s AEIOU-TIPS H’s and T’s Corresponding H’s and T’s A Alcohol T Toxins E Epilepsy or seizure, endocrine H/T Hydrogen / Thrombosis (neuro) I Infection N/A N/A O Overdose T Toxins U Uremia N/A N/A T Trauma, blood loss, shock H Hypovolemia I Insulin H Hypoglycemia P Poisoning / Psychiatric T Toxins S Stroke, Syncope T Thrombosis Stroke / CVA • Annually, more than 795,000 people in the United States have a stroke. – Of these 610,000 are first or new strokes • More than 130,000 Americans die each year as a result of stroke • Every 40 seconds, someone in the U.S. has a stroke, and every 4 minutes someone in the U.S. dies from a stroke • Hypertension, high cholesterol, and smoking are the leading causes of stroke – Symptom presentation alone is not definitive in differentiating ischemic from hemorrhagic stroke FAST Exam • Rapid, 4-step approach to evaluation for potential stroke • Should be performed on any patient presenting with stroke-like symptoms, regardless of time of onset • Research has shown that the FAST exam has up to an 85% sensitivity for stroke • Other stroke screening methods include the Los Angeles Prehospital Stroke Screen (LAPSS), Cincinnati Prehospital Stroke Scale (CPSS), and the NIH Stroke Scale (NIHSS) FAST Exam - Components • Face – Ask the patient to smile. Observe for facial droop • Arm – Have the patient raise both arms out in front of them and close their eyes. Observe for arm drift or fall • Speech – Ask the patient to repeat a simple phrase. Observe for slurring of speech or other speech abnormalities • Time – Remember that TIME IS BRAIN! If possible, obtain the time of symptom onset or the time last known well. – For the general public, this component instructs them to call 911 if any of the other components of the screening are abnormal. Ischemic vs Hemorrhagic Stroke • Ischemic strokes result from interruption of blood flow to the brain tissues caused by a clot • Hemorrhagic stroke results from a vascular defect that causes bleeding around or into the brain tissue. – Aneurysmal • Berry / Saccular – Form along the artery, including bifurcations, and resemble a berry growing from a twig • Fusiform – Form along the artery and encompass the vessel circumferentially – Traumatic injury with vascular rupture – Spontaneous Ischemic Stroke • Accounts for 80% of all strokes – 2 Sub-types • Thrombotic – Result from the formation of a clot within the vasculature of the brain itself, often caused by atherosclerosis or plaque build up (much like myocardial infarction) • Embolic – Result from the formation of a clot somewhere in the body that travels to the brain and occludes blood flow – Characterized by an area of acute ischemia due to lack of blood flow, and a surrounding area of limited or decreased perfusion called the ischemic penumbra – In 5% of cases, hemorrhagic conversion occurs as a result of capillary leaking or disruption of the blood-brain barrier – Initially, CT may appear normal due to lack of sensitivity for infarcted tissue. Later CT studies will show areas of infarct and loss of gray/white mater differentiation Ischemic Stroke • History, Signs, & Symptoms – Patients with risk factors for cardiac and atherosclerotic disease are also at risk for ischemic stroke • Hypertension, diabetes, tobacco use, high cholesterol, and history of CAD, CABG, and/or Atrial fibrillation – Stroke should be considered in any patient with acute neurologic deficit (global or focal), or altered level of consciousness – Abrupt onset of the following: • Hemiparesis, monoparesis, hemisensory deficits, monocular or binocular vision loss, visual field deficits, diplopia (double vision), dysarthria (difficult or unclear articulation of speech), facial droop, ataxia (loss of full control of body movements), vertigo, aphasia (loss of ability to understand or express speech), and/or sudden decrease in level of consciousness – Symptoms can appear alone, however they are more likely to appear in combination – History of Transient Ischemic Attack (TIA) increases a patient’s risk of a true ischemic stroke Post-mortem exam of an ischemic stroke. Note the obviously infarcted brain tissue. Ischemic Stroke • Treatment – Thorough history and physical – OBTAIN TIME LAST KNOWN WELL • Thrombolytic therapy must be done within 4-6 hours postonset of symptoms. This window is being extended by some facilities, but typically <4 hours is standard. – GLASGOW COMA SCORE – FAST EXAM – Initial Medical Care – Blood glucose level – 12-lead ECG – Vascular Access / Cardiac Monitoring – Be alert for subtle mental status changes – Rapid transport and notification of receiving facility • Stroke Alert Ischemic Stroke - tPA • A pharmacologic option for treating ischemic stroke patients is the use of tissue plasminogen activator (tPA), a.k.a Activase® • Not routinely administered in the prehospital environment • Works by promoting thrombolysis through the conversion of plasminogen to plasmin; plasmin degrades fibrin and fibrinogen, resulting in breakdown of the clot. Ischemic Stroke - tPA • Contraindications: – Active internal bleeding – Current intracranial hemorrhage – Intracranial neoplasm, arteriovenous malformation, aneurysm, or any other condition that may increase bleeding risk – Recent intracranial or spinal surgery (within 3 months) – Recent head trauma (within 3 months) – Severe uncontrolled hypertension Ischemic Stroke - tPA • Dosing: – 0.9 mg/kg IV • 10% of total dose is given as a bolus over one minute • Remainder is administered via IV infusion over 60 minutes • MAX total dose 90mg – Should be administered with 3 – 4.5 hours of symptom onset, although can be given up to 6 hours post-symptom onset in certain situations as deemed appropriate by a physician Ischemic Stroke - tPA • Adverse Effects – – – – – – – – – Hemorrhage Anaphylaxis CVA / Intracranial hemorrhage Seizure Angioedema Cardiac dysrhythmia Cardiac tamponade Cerebral herniation Pulmonary edema Types of Hemorrhagic Stroke • Epidural – Usually results from trauma to the temporal region of the skull – Commonly caused by a rupture of the middle meningeal artery – Causes bleeding between the skull and dura mater (hence epidural, meaning above the dura) – Only accounts for roughly 2% of strokes – CT shows ‘typical’ crescent shaped area of bleeding Epidural Hematoma • History, Signs, & Symptoms – Trauma is usually involved, but not always • History of direct blow to the head, usually to the temporal or parietal area • Can also be related to hypertension, vascular malformation, anticoagulant therapy – “Classic” presentation is immediate loss of consciousness, followed by a lucid interval during which the patient is conscious, and then a precipitous decline in mental status and level of consciousness, progressing to coma – Symptoms may include headache, nausea, vomiting, seizures, focal neurologic deficit, weakness, numbness, and urinary or fecal incontinence – Bradycardia, hypertension, and irregular respirations (Cushing’s Triad) may be present as intracranial pressure increases Note the dura mater is still intact, and the hematoma is resting on it Epidural Hematoma • Treatment – – – – – – – – – – Thorough history and physical Spinal motion restriction as required and needed Ascertain the mechanism and time of injury Obtain time last known well GLASGOW COMA SCORE FAST exam Initial Medical Care Vascular Access / Cardiac Monitoring Be alert for subtle mental status changes Rapid transport and notification of receiving facility – Acute epidural hematomas, depending on size and neurologic deficit, are a surgical emergency Types of Hemorrhagic Stroke • Subdural – Commonly caused by trauma, but not always! – Can be acute, subacute, or chronic – Bleeding occurs below the dura mater but above the arachnoid mater • Usually venous bleeding, but can be arterial • Damage to the bridging vessels between the surface of the brain and the dura – Accounts for 5 – 25% of hemorrhagic strokes and cerebral hematomas – CT shows bleeding that follows the contour of the brain in a ‘wavy’ appearance Subdural Hematoma • History, Signs, & Symptoms – Commonly caused by trauma, but not always! • Rapid acceleration / deceleration forces cause shearing of vasculature • Can also be caused by hypertension, anticoagulant therapy, cerebral aneurysms, arteriovenous malformations, or spontaneous – Clinical presentation depends on the location of the lesion and the rate at which it develops – Signs and symptoms resemble other hemorrhagic strokes • Headache, nausea, vomiting, drowsiness, dizziness, confusion, unequal pupil size, slurred speech, hypertension, lethargy, seizures, coma – Bradycardia, hypertension, and irregular respirations (Cushing’s Triad) may be present as intracranial pressure increases Note the dura mater has been surgically resected, revealing the subdural hematoma Subdural Hematoma • Treatment – – – – – – – – – – – Thorough history and physical Spinal motion restriction as required and needed Ascertain the mechanism and time of injury if applicable Obtain time last known well GLASGOW COMA SCORE FAST exam Initial Medical Care Vascular Access / Cardiac Monitoring Be alert for subtle mental status changes Rapid transport and notification of receiving facility Symptom onset will vary based on the rate of progression of the bleed • Acute – Typical symptom onset immediately following injury up to 4 days postinjury • Sub-Acute – Typical symptom onset 4 – 21 days after injury • Chronic – Typical symptom onset > 21 days post-injury Types of Hemorrhagic Stroke • Subarachnoid Hemorrhage – Can be caused by trauma or spontaneous aneurysmal rupture – Results in bleeding beneath the arachnoid mater but above the pia mater – CT shows blood present in the fissures of the brain, giving the bleed a spider-like appearance Subarachnoid Hemorrhage • History, Signs, & Symptoms – Can be traumatic or caused by rupture of a cerebral aneurysm or arteriovenous malformation, or neoplastic growth • 80% are due to ruptured berry or saccular aneurysms – “Classic” presentation is a sudden onset headache (‘thunderclap headache’) often described as the worst of their life, nausea, vomiting, and signs of meningeal irritation (nuchal rigidity, neck pain, back pain, and/or bilateral leg pain) – Dizziness, orbital pain, diplopia (double vision), visual loss, sensory or motor disturbances, seizures, ptosis (drooping of the upper eyelid), memory loss, dysphasia, and/or seizure – Hypertension is common – Bradycardia, hypertension, and irregular respirations (Cushing’s Triad) may be present as intracranial pressure increases Post-mortem examination of a SAH. Note blood is present around the Circle of Willis, outside the pia mater. Subarachnoid Hemorrhage • Treatment – – – – – – – – – – – – Thorough history and physical Spinal motion restriction as required and needed Ascertain the mechanism and time of injury if applicable Obtain time last known well GLASGOW COMA SCORE FAST exam Initial Medical Care Vascular Access / Cardiac Monitoring Monitor blood pressure closely Be alert for subtle mental status changes Rapid transport and notification of receiving facility Symptom onset will vary based on the rate of progression of the bleed Types of Hemorrhagic Stroke • Intraparenchymal / Intracerebral Hemorrhage – Most commonly caused by leaking blood vessels within the brain tissue itself; can also be caused by spontaneous rupture of blood vessels – Results in bleeding within the brain tissue itself, under the pia mater – Accounts for 10% of all hemorrhagic strokes – CT shows accumulation of blood in the intracerebral space that does not follow the contour of the meninges and may appear circular in shape Intraparenchymal / Intracerebral Hemorrhage • History, Signs, & Symptoms – Often due to spontaneous rupture or leak from an intracerebral vessel – Hemiparesis, hemisensory loss, right or left gaze preference, visual field cut, aphasia, atypical neglect, gait or limb ataxia, vertigo, nausea, vomiting, seizure, and coma – Hypertension is common, with measurements of 200/120mmHg seen – Bradycardia, hypertension, and irregular respirations (Cushing’s Triad) may be present as intracranial pressure increases Post-mortem exam of an intracerebral hemorrhage. Note the accumulation of blood in a spherical shape within the brain tissue. Intraparenchymal / Intracerebral Hemorrhage • Treatment – – – – – – – – – – – Thorough history and physical Spinal motion restriction as required and needed Ascertain the mechanism and time of injury if applicable Obtain time last known well GLASGOW COMA SCORE FAST exam Initial Medical Care Vascular Access / Cardiac Monitoring Monitor blood pressure closely Be alert for subtle mental status changes Rapid transport and notification of receiving facility Applying SOP’s to Altered Mental Status • Adult IMC (SOP p. 4-5) – Initial baseline assessment of patient and care of life-threatening emergencies. – Begin more in-depth assessment of patient to identify causes of emergency / mental status changes. • i.e. MI / Hypoxia / Hypoglycemia Applying SOP’s to Altered Mental Status • Adult Suspected Cardiac Patient with Chest Pain (SOP p. 12) – BLS • Adult IMC (SOP p. 4-5) • Rapid transport – ALS • Chest pain mental status change causes – Bradydysrhythmia (SOP p. 15) – Cardiogenic shock (SOP p. 23) Applying SOP’s to Altered Mental Status • Adult Bradydysrhythmia (SOP p. 15) – Unstable: Altered Mental Status • Causes of altered mental status – Decreased perfusion (CO = SV x HR) • Treatment: Supraventricular bradycardia/ 2nd degree Type 1 blocks • Atropine until pacing available • Corrective goal = Increased HR • Transcutaneous pacing • Corrective goal = Increased HR Applying SOP’s to Altered Mental Status • Adult Bradydysrhythmia cont. (SOP p. 15) – Unstable: Altered Mental Status • Causes of altered mental status – Decreased perfusion (CO = SV x HR) • Treatment: 2nd degree Type 2 / 3rd degree blocks • Transcutaneous pacing • Corrective goal = Increased HR • Transcutaneous pacing • Corrective goal = Increased HR Applying SOP’s to Altered Mental Status • Adult Supraventricular Tachycardia (SOP p. 16) – Unstable: Altered Mental Status • Causes of altered mental status – Decreased preload in the heart (not enough filling time) • Treatment: HR > 150 BPM • Synchronized cardioversion(s) • Corrective goal = Allow the heart to restart at a normal intrinsic rate (60-100 BPM), thus increased the preload timing of the heart. Applying SOP’s to Altered Mental Status • Adult Ventricular Tachycardia with a pulse (SOP p. 17) – Unstable: Altered Mental Status • Causes of altered mental status – Decreased preload in the heart (not enough filling time) • Treatment: HR > 150 BPM wide complex • Synchronized cardioversion(s) • Corrective goal = Allow the heart to restart at a normal intrinsic rate (60-100 BPM), thus increased the preload timing of the heart. • Amiodarone 150mg / 10 minutes IV/IO • Corrective goal = Increasing preload / ventricular filling time by increasing the cardiac refractory period. Applying SOP’s to Altered Mental Status • Adult Ventricular Tachycardia without a pulse / Ventricular Fibrillation (SOP p. 19) – Unstable: Altered Mental Status / Cardiac Arrest • Causes of altered mental status – Cardiac arrest / no heartbeat • Treatment • Defibrillation / CPR • Corrective goal = Restart the heart / increase cerebral perfusion. • Amiodarone 300 mg IV/IO • Corrective goal = Increasing preload / ventricular filling time by increasing the cardiac refractory period. Applying SOP’s to Altered Mental Status • Adult Asystole / PEA (SOP p. 21) – Unstable: Altered Mental Status / Cardiac Arrest • Causes of altered mental status – Cardiac arrest / no heartbeat • Treatment • CPR • Corrective goal = Restart the heart / increase cerebral perfusion. • Epinephrine 1mg 1:10000 IV/IO • Corrective goal = Stimulates alpha and beta receptors, can also increase coronary and cerebral perfusion pressures during CPR. Applying SOP’s to Altered Mental Status • Adult Pulmonary Edema (due to heart failure) (SOP p. 22) – Unstable: Altered Mental Status • Causes of altered mental status – Hypoxia • Treatment • High FiO2 or ventilation • Corrective goal = increasing adequate ventilation and positive end expiratory pressures • Depending on HR • Bradydysrhythmia SOP (HR < 60 BMP) • Cardiogenic Shock SOP (HR > 60 BPM) Applying SOP’s to Altered Mental Status • Adult Cardiogenic Shock (SOP p. 23) – Unstable: Altered Mental Status • Causes of altered mental status – Hypoxia / Decreased cardiac output • Treatment • IV Fluid bolus, 200 ml increments • Corrective goal = Increase cardiac output by increasing preload • Dopamine infusion • Corrective goal = Increase HR (chronotropic effect), thus increase CO ( CO= SV x HR) • Corrective goal = Increase CO (intopropic effect) by increasing cardiac contractility Applying SOP’s to Altered Mental Status • Adult Airway Obstruction (SOP p. 24) – Stable / Unstable with Altered Mental Status • Causes of altered mental status – Hypoxia / hypercarbia • Treatment • Clear airway / bypass obstruction • Corrective goal = Increase ventilation and removal of hypercarbic gases Applying SOP’s to Altered Mental Status • Adult Asthma / COPD (SOP p. 27) – Stable / Unstable with Altered Mental Status • Causes of altered mental status – Hypoxia / hypercarbia • Treatment • Albuterol 2.5 mg / 3ml • Corrective goal = Increase pulmonary structures to allow better gas exchange • CPAP / NIPPV • Corrective goal = Decrease work of breathing, aid ventilation, increase positive end expiratory pressures (PEEP) • Epinephrine 1:1000 0.3 mg IM • Corrective goal = Increase bronchodilation Applying SOP’s to Altered Mental Status • Adult Partial Upper Airway Obstruction / Epiglottitis (SOP p. 28) – Unstable: Altered Mental Status • Causes of altered mental status – Hypoxia / hypercarbia • Treatment • Epinephrine 1:1000 3 mg (3ml) via nebulizer • Corrective goal = Increase bronchodilation by relaxing smooth muscles. • Non-breathing • High FiO2 ventilation • Corrective goal = Increase ventilations, increase oxygenation and gas exchange Applying SOP’s to Altered Mental Status • Adult Allergic Reaction / Anaphylaxis (SOP p. 29) – Stable / Unstable with Altered Mental Status • Causes of altered mental status – Hypoxia / hypercarbia / Vasodilation • Treatment • IV Fluid Bolus • Corrective goal = Increase BP / CO • Epinephrine 1:10000 IV/IO 0.1 mg IV/IO up to 0.5 mg total q 3 minutes based on Pt. condition • Corrective goal = Vasodilation / Bronchodilation • Epinephrine 1:1000 0.3 mg IM • Corrective goal = Increase bronchodilation Applying SOP’s to Altered Mental Status • Adult Allergic Reaction / Anaphylaxis cont. (SOP p. 29) • Treatment • Benadryl 50 mg IV / IO (IM if no IV/IO) • Corrective goal = Blocking histamine-1 uptake at the receptor sites • Albuterol 2.5 mg / 3 ml via nebulizer • Corrective goal = Bronchodilation • Dopamine • Corrective goal = Increase HR (chronotropic effect), thus increase CO ( CO= SV x HR) • Corrective goal = Increase CO (inotropic effect) by increasing cardiac contractility • Corrective goal = Increase vasoconstriction Applying SOP’s to Altered Mental Status • Adult Diabetic / Glucose (SOP p. 30) – Unstable: Altered Mental Status • Causes of altered mental status – Hypo / Hyperglycemia • Treatment • Hypoglycemia • Dextrose 50% 25 g IV or Glucagon 1 mg IM no IV • Corrective goal = Increase blood glucose levels to facilitate metabolic energy production • Hyperglycemia • IV fluid bolus(es) • Dilute blood glucose levels Applying SOP’s to Altered Mental Status • Adult Syncope / Near Syncope (SOP p. 31) – Unstable: Altered Mental Status • Causes of altered mental status – H’s and T’s / AEIOU-TIPS – Opioids • Treatment • Narcan • BLS 2 mg IN / ALS 1 mg IV/IN repeated at 0.5 mg q 2 minutes up to 2 mg total • Corrective goal = Increase ventilatory rates without causing withdrawal Applying SOP’s to Altered Mental Status • Adult Seizure / Status Epilepticus (SOP p. 32) – Unstable: Altered Mental Status • Causes of altered mental status – Seizure activity causing inadequate respirations / non coordinated neurological activities • Treatment • If actively seizing • Versed 2 mg slow IV/IO q 2 minutes up to 10 mg as needed. No IV, < 70 lbs 5 mg IM, > 70 lbs 10 mg IM. • Corrective goal = Stop the seizure by acting as a CNS depressant with anticonvulsant effects. Applying SOP’s to Altered Mental Status • Adult Stroke (SOP p. 33) – Unstable: Altered Mental Status • Causes of altered mental status – Ischemic stoke causing cerebral hypoxia – Hemorrhagic stroke causing compression or changes in blood flow • Treatment • Maintain head in neutral alignment • Corrective goal = Facilitate blood flow for ischemic strokes (increase cerebral perfusion pressures). Hemorrhagic stoke, increase bilateral venous drainage • Elevate head of bed 15-30 degrees • prevent excessive drainage / flow Applying SOP’s to Altered Mental Status • Adult Stroke cont. (SOP p. 33) • Treatment • Obtain last know normal • Corrective goal = Allow receiving facility to better prepare if the patient is eligible for intervention • Elevate head of bed 15-30 degrees • Corrective goal = Prevent excessive drainage / flow • Intubation (GCS < 8) • Corrective goal = Protect the patient against aspiration and ensure adequate ventilation and gas exchange Applying SOP’s to Altered Mental Status • Adult Acute Abdominal Pain (SOP p. 34) – Unstable: Altered Mental Status • Causes of altered mental status – Decreases in adequate circulation preventing oxygenation • Treatment • Large bore IV – IV Fluid Bolus(es) of 200 ml • Corrective goal = Increase volume to ensure proper global circulation of hemoglobin to help perfuse vital organs. Applying SOP’s to Altered Mental Status • Adult Toxicological (SOP p. 35) – Unstable: Altered Mental Status • Causes of altered mental status – Substances causing decreased mentation – Inadequate cardiac activities decreasing circulation • Treatment / Opioids • Narcan • BLS 2 mg IN / ALS 1 mg IV/IN repeated at 0.5 mg q 2 minutes up to 2 mg total • Corrective goal = Increase ventilatory rates without causes withdrawal Applying SOP’s to Altered Mental Status • Adult Toxicological cont. (SOP p. 35) • Treatment: Cyclic antidepressants / Sodium channel blocker overdose • Normal Saline 1 L IV Bolus • Corrective goal = Increase circulating volume to increase blood pressures • Corrective goal = Slowing the uptake of antidepressants are the receptor sites. • Treatment: Beta-Blocker / Calcium channel blockers • Glucagon 1 mg slow IV • Corrective goal = Positive inotropic (increase contractility) and chronotropic (increase rate) effects Applying SOP’s to Altered Mental Status • Adult Toxicological cont. (SOP p. 36) • Treatment: Cyanide Poisoning • Consider NIPPV / CPAP / Advanced Airway • Corrective goal = Increase intrathoracic pressures and aid in ventilation / respiration • Hydroxocobalamin 5 g over 15 minutes IV (if available) • Corrective goal = Rapid resolution of cyanideinduced lactic acidemia. Applying SOP’s to Altered Mental Status • Adult Chronic Renal Failure (SOP p. 43) – Unstable: Altered Mental Status • Causes of altered mental status – Electrolyte imbalances / changes in cardiac output – Acidosis impeding the hemoglobin's ability to bind with oxygen • Treatment • Sodium Bicarbonate 1 mEq/kg IV/IO • Corrective goal = Buffer acidosis and raises serum pH (hyperkalemia causes acidosis) Glucagon MEDICATION OF THE MONTH Medication Of The Month • Glucagon (GlucaGen) – Classification • Hormone, anti-hypoglycemic agent – Indications • Hypoglycemia patients without venous access • Beta or calcium channel blocker overdose with symptomatic bradycardias including AV blocks (dosage required usually exceeds that available in pre-hospital setting) – Actions • Causes a breakdown of stored glycogen into glucose • Independent of beta blockage, positive inotropic and chronotropic and improved AV conduction. Medication Of The Month • Glucagon (GlucaGen) – Diabetic / Glucose Emergencies • Adult – 1 mg IM • Pediatric – > 8 years: 1 mg IM – < 8 years: 0.5 mg IM – Beta / Calcium Channel Blocker Overdose • Adult – 1 mg slow IV/IO, may repeat x 1 • Pediatric – 0.5 mg IV/IO, may repeat x 1 Medication Of The Month • Glucagon (GlucaGen) – Contraindications • Hypersensitivity to glucagon or proteins – Side Effects • • • • Nausea Vomiting Dizziness Headache CARDIAC RHYTHM OF THE MONTH Dysrhythmias • Hyperkalemic ECG changes – As serum potassium rises (may be seen in chronic renal failure patients) the hearts ability to correctly depolarize becomes impaired. If uncorrected, cardiac arrest may occur as potassium levels continue to rise. CAPNO WAVEFORM OF THE MONTH Capno Waveform • ETCO2 monitoring – – – – A-B = no air movement / respiratory baseline B-C = expiratory upslope -> “dead space” air, followed by distal bronchi C-D = expiratory plateau -> alveolar gases being measured D-E = inspiratory downstroke -> inhalation begins Capno Waveform • ETCO2 monitoring – Reverse “shark-fin” • Can only be seen on non-intubated patients – Expiration is less impaired than inspiration • Inspiratory downstoke is delayed secondary to underlying condition Capno Waveform • ETCO2 monitoring – Causes • Epiglottis • Stridor secondary to: – Anaphylaxis – Allergic Reaction – Upper airway inhalation injuries Scenario • You are dispatched for a 48 year old male, reported to be unresponsive. You have no history at this address. PD is with the patient and the scene is secure. You have your partner and an engine company (1 Paramedic, 2 EMT-B’s) with you. • When you arrive the patient is noted to be laying on the floor. – – – – A - snoring respirations. B - Irregular respirations. C - Pt. has a bounding pulse, no obvious hemorrhage D - Eyes open to pain, Verbal incomprehensible sounds, M withdraws Scenario • Wife states that the Pt. was “acting weird” then collapsed – No medications – No allergies – No history • Head to toe – No obvious S/S of trauma. Cap refill 3 seconds. Global inspection unremarkable with the exception of the head with: • Pupils pinpoint. All other findings WNL – When asked about drug use wife states she has never known the Pt. to use drugs • V/S obtained – – – – – – – – Resp: B/P: HR: Skin: Pupils: Lungs: Dexi: ETCO2: 26 Irregular 204/120 58 WNL X 3 Pinpoint at 2mm bilaterally, minimally reactive Clear 102 32 mmHg Scenario • What is your initial course of action for this patient after Adult IMC (Sop. 4)? Ventilations Narcan CPR Stroke Care Rapid Transport Intubation Refusal Dextrose Ventilations • You assist the patient with a BMV utilizing the C and E clamp method – Respiratory depth and quality improves – Practice ventilating a mannequin with the C-E clamp technique Narcan • You consider the use of Narcan with the decrease mental status and pinpoint pupils, however, your index of suspicion of drug use is low. – Should you administer Narcan, what is your dose and route – Practice administering Narcan with a MAD device CPR • Since the patient has a pulse and blood pressure, CPR is not indicated for this patient. https://vimeo.com/172042262 – Remember, 100 compressions / minute is the goal Stroke Care • This patient exhibits S/S of a possible stroke, including crushing's triad. What are the BLS and ALS interventions for this patient? – – – – HOB elevation Neutral alignment of neck Obtaining last know well Airway protection (decrease GCS) • What medications for DAI? • What is your targeted ETCO2 levels? Intubation • Adult IMC (SOP pg 4) • High FIO2 ventilation assist – CE Clamp • Benzocaine spray (0.5-1 second spray x 2) • CDH / Edward – Ketamine • 1mg/kg slow IV/IO • Loyola / Good Sam – Etomidate • 0.6 mg/kg IV/IO push over 30-60 seconds, max dose 40 mg • • • Confirm ETT placement, secure Apply ETCO2 monitoring, ventilate to ETCO2 of 35-45 (30-35 with S/S of herniation. Post intubation sedation Rapid Transport • Adult IMC (SOP pg 4) • Ensure that your basic life threats are addressed prior to transporting. – Ensure your ABCD’s are sustainable to life • • • • A – Airway – Assist Ventilations B – Breathing – Ensure adequate rate and quality C – Circulation - Pulse is present D – Disability – Establish a baseline mental status • Document last know well • Ensure the right patient is going to the right facility Refusal • Based on the initial assessment, this patient is not able to obtain a refusal. Dextrose • Based on the patient having no history of diabetes and a blood sugar of 102, dextrose is not indicated for this patient.