Altered Mental Status / Stroke

Altered Mental Status / Stroke
Region 8 EMSS April 2017 Altered Mental Status / Stroke

Objectives Define altered mental status Define stroke Review Causes
Review Corrections Review Treatment Define stroke

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 Confused Localizes Pain 2 Opens to Pain Inappropriate Withdraws From Pain 1 No Opening Incomprehensible Sounds Decorticate Posturing No Verbal Sounds Decerebrate Posturing No Movement AVPU is a quick assessment tool that can establish mental status

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 AVPU is a quick assessment tool that can establish mental status

AVPU vs. GCS AVPU GCS Ranges Alert 15 Verbal 4-14 Painful 4-10 Unresponsive 3 AVPU is a quick assessment tool that can establish mental status 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 Alcohol E Epilepsy or seizure, endocrine I Infection O Overdose (opiates) U Uremia T Trauma, blood loss, shock I Insulin P Poisoning/psychiatric S Stroke, syncope Although all potential causes should be considered the above pneumonic helps to address the most common causes.

Altered Mental Status H’s and T’s
H Hypovolemia H Hypoxia H Hydrogen Ion H Hypo/Hyperkalemia H Hypothermia T Tension pneumothorax T Tamponade / cardiac T Toxins T Thrombosis, pulmonary (PE) T Thrombosis, cardiac / neuro Although all potential causes should be considered the above pneumonic helps to address the most common causes.

AEIOU-TIPS vs H’s and T’s AEIOU-TIPS Corresponding H’s and T’s H’s and T’s A Alcohol T Toxins E Epilepsy or seizure, endocrine H / T Hydrogen / Thrombosis (neuro) I Infection N/A O Overdose U Uremia Trauma, blood loss, shock H Hypovolemia Insulin Hypoglycemia P Poisoning / Psychiatric S Stroke, Syncope Thrombosis Although all potential causes should be considered the above pneumonic helps to address the most common causes.

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 Annually, strokes cost the United States over $33 billion, which includes the cost of healthcare services, medications to treat stroke, and missed days of work

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 Arm Speech Time
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 post-onset 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 pre-hospital environment Works by promoting thrombolysis through the conversion of plasminogen to plasmin; plasmin degrades fibrin and fibrinogen, resulting in breakdown of the clot. CDH MSU has the ability to initiate tPA under on-line direction of an interventional neurologist following CT scan

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

Note the dura mater is still intact, and the hematoma is resting on it
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

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 post-injury Sub-Acute Typical symptom onset 4 – 21 days after injury Chronic Typical symptom onset > 21 days post-injury

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

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

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)

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 CO = HR x SV. With a decreased in HR a decreased in CO is noted. Attempt to improve CO by increased HR with medications and or pacing.

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 CO = HR x SV. With a decreased in HR a decreased in CO is noted. Attempt to improve CO by increased HR with medications and or pacing.

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 ( BPM), thus increased the preload timing of the heart. CO = HR x SV. With a decreased in HR a decreased in CO is noted. Attempt to improve CO by increased HR with medications and or pacing.

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 ( 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. CO = HR x SV. With a decreased in HR a decreased in CO is noted. Attempt to improve CO by increased HR with medications and or pacing.

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.

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.

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)

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

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

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: mg IM Corrective goal = Increase bronchodilation

Adult Partial Upper Airway Obstruction / Epiglottitis (SOP p. 28) Unstable: Altered Mental Status Causes of altered mental status Hypoxia / hypercarbia Treatment Epinephrine 1: 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

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: mg IM Corrective goal = Increase bronchodilation

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

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

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

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.

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 degrees prevent excessive drainage / flow

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 degrees Corrective goal = Prevent excessive drainage / flow Intubation (GCS < 8) Corrective goal = Protect the patient against aspiration and ensure adequate ventilation and gas exchange

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.

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

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

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 cyanide-induced lactic acidemia.

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)

Medication of the month
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.

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 1 mg slow IV/IO, may repeat x 1 0.5 mg IV/IO, may repeat x 1

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: 26 Irregular B/P: 204/120 HR: 58 Skin: WNL X 3 Pupils: Pinpoint at 2mm bilaterally, minimally reactive Lungs: Clear Dexi: 102 ETCO2: 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 https://vimeo.com/172042262
Since the patient has a pulse and blood pressure, CPR is not indicated for this patient. 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 seconds, max dose 40 mg Confirm ETT placement, secure Apply ETCO2 monitoring, ventilate to ETCO2 of (30-35 with S/S of herniation. Post intubation sedation

Rapid Transport Document last know well
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.

Altered Mental Status / Stroke

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