1. Angina, Acute MI, & Acute Stroke
August 2014 CE
Condell Medical Center EMS System
Prepared by: Sharon Hopkins, RN, EMT-P, BSN
Rev

2. Objectives
Upon successful completion of this module, the EMS provider will be able to:
1. Describe the pathophysiology of angina.
2. Describe the pathophysiology of the acute
myocardial infarction process.
3. Describe the atypical presentations of women,
elderly, and those with long standing diabetes.

3. Objectives cont’d 4. Describe the pathophysiology of ischemic and
hemorrhagic strokes.
5. Describe field assessment of the patient
with a possible stroke including documentation of
time of onset, blood sugar level, and Cincinnati
Stroke Scale.
6. Actively participate in review of selected Region X
SOP’s.

4. Objectives cont’d
7. Actively participate in review of a variety of EKG
rhythms and 12 lead EKG’s.
8. Actively participate in case scenario discussion.
9. Actively participate in calculating and
preparing medication doses for the pediatric
patient.
10. Review responsibilities of the preceptor role.
11. Successfully complete the post quiz with a score
of 80% or better

5. Cardiovascular Anatomy
Cardiovascular system has 2 major components
Heart
4 chambered pump
2/3 of mass is to left of sternum
Apex just above diaphragm
Base, top of heart, lies at level of 2nd rib
Peripheral blood vessels
Transport system to deliver blood to the body and to transport waste for removal

6. Layers of the Heart Pericardium – protective sac around heart
Epicardium - Outer most layer
Coronary vessels lie on this epicardial layer
Myocardium
Thick middle layer of cells with electrical properties
Endocardium - Inner most layer
Lines heart chambers; in contact with blood flow within the chambers

7. Cardiac Damage Post MI Each individual is unique
Damage may be only on the surface or penetrate all layers of the heart
The greater the level/degree of damage to the heart the more negatively affected the heart is to work as a pump

8. Diagram of the Heart

9. What is Acute Coronary Syndrome (ACS)?
A list of diagnoses that affect the cardiac system
Indicates an interruption of blood flow to the heart
Unstable angina
Non-ST elevation MI
ST elevation MI

10. What Causes ACS To Develop?
An imbalance between supply and demand of O2
Atherosclerotic plaque rupture in coronary artery
Thrombosis (clot) formation in artery
Coronary spasm
Dissection of blood vessel
Increased demand of O2 in face of fixed obstruction

11. Main Contributing Risk Factors to Cardiac Problems
Hypertension
Hyperlipidemia
Smoking
Diabetes
Notice: all of the above are considered modifiable risk factors – you can do something to control them!

12. Pathophysiology of angina
Chest pain/discomfort related to a decrease in oxygen-rich blood flow
Usually due to coronary artery disease (CAD)
Atherosclerosis
Build up of plaque over time that narrows the internal diameter of the vessel
Arteriosclerosis
Stiffening of vessels over a period of time which makes them less pliable

13. Pathophysiology of Angina
Plaque formation
Angina serves as a warning that something is going on

14. Stable Angina Most common form
Pain occurs when oxygen demand is greater than the supply during periods of increased workload of the heart
Can usually predict activities that will trigger an event
Usually treated with rest and medication (i.e.: nitroglycerin)
This is a warning that the patient may have an acute MI in the future

15. Unstable Angina Pain that is unpredictable and can occur at rest
May not stop with rest and/or medication
Event to be taken seriously
May be predicting an imminent acute MI in the near future

16. Variant Angina Occurs when vessel is in spasm Very painful
Often occurs at night
Controlled with medication

17. Treating Angina
Treated as if the patient were experiencing an acute MI
Patient should stop activity and rest
Question if the patient has taken their own nitroglycerin or other medication
Often, if the pain is relieved with rest and nitroglycerin, it is usually angina, not acute MI

18. Pathophysiology of Acute MI Process
Significant blockage of one or more coronary arteries
Atherosclerosis is gradual process, typically over decades, of plaque build-up on arterial walls
Size and area affected impacts outcome
Location, location, location!

19. Development of Blockage

20. Ischemic Cascade Heart cells around blocked coronary artery die
These do not regenerate
Collagen scar forms
Scarring increases risks for potentially life-threatening dysrhythmias
Weakened muscle walls vulnerable to formation of ventricular aneurysm which could rupture at any time
Injured heart tissue conducts electrical impulses more slowly
Allows for possible development of re-entry or feedback loop that can generate dysrhythmia

21. Pathological Types of Acute MI
Transmural – atherosclerosis affected a major coronary artery
MI extends through whole thickness of heart muscle
Anterior, posterior, inferior, lateral, septal walls
ST elevation noted on EKG and Q waves develop
Subendocardial
Small area below surface of wall involved in left ventricle, ventricular septum, or papillary muscle
ST depression noted on EKG

22. Coronary Circulation Coronary arteries (CA)
Vessels that originate in aorta
Supply the heart with it’s blood flow
Main CA lies on surface of heart – epicardial coronary arteries
Small penetrating arteries supply myocardial muscle

23. Collateral Circulation
Protective mechanism to provide alternative path for blood flow in case of system blockage
Takes time to develop

24. Coronary Arteries Left coronary artery 2 branches Left ventricle
Interventricular septum
Part of right ventricle
Heart’s conduction system
2 branches
Anterior descending artery (LAD)
Circumflex artery

25. Coronary Arteries cont’d
Right coronary artery
Portion right atrium, right ventricle, and part of conduction system
2 branches
posterior descending artery
Marginal artery

26. STEMI Waveform Pattern
Evaluation of ST segment elevation
0.04 seconds after J point
>2mm for males in V2 and V3
>1.5mm females in V2 and V3
>1mm in other EKG leads
Early STEMI may just display peaked T wave
ST elevation develops later

27. Elements of AMI

28. Myocardium and Vessel Structure
Notice that coronary arteries lie on epicardial surface

29. Patient Complaints and Evaluation
Symptoms that persist beyond 15 minutes
Remember that symptoms may be vague
Always consider worse case scenario and hope for the best
When in doubt, obtain a 12 lead EKG
Remember: a negative 12 lead EKG does not mean the patient is NOT having an MI
We are just positive when ST elevation is present

30. Mimics of Chest Pain Occurrences of chest pain must be fully evaluated
Assume the worst; hope for the best
Need to consider other differential diagnosis putting the one that is most life threatening at the top of the list
Remember to not be fooled by atypical presentation of AMI

31. Differential Diagnosis …What Could This Be???
Stable angina
Acute pericarditis
Aortic dissection
Pulmonary embolism
Pneumonia
Pneumothorax
Esophageal spasm
Reflux
Gastritis
Cholecystitis
Pancreatitis
Musculoskeletal pain

32. Non-atherosclerotic Causes AMI in Younger Patients
Emboli from infected cardiac valves
Coronary occlusion from vasculitis
Coronary artery spasms
Cocaine use
Congenital coronary anomalies
Coronary trauma
Increased O2 requirement
Decreased O2 delivery (i.e.: anemia)

33. Typical Patterns of Chest Pain May be from surge of catecholamines in response to pain and hemodynamic abnormalities from cardiac dysfunction

34. Atypical Presentations
Women, elderly, long standing diabetics
Back pain
Jaw pain
Right arm pain
Indigestion
Nausea
Fatigue/weakness
Dyspnea/ shortness of breath
No pain

35. Atypical Presentation in Women
Most frequent complaints in women are shortness of breath, weakness, feeling of indigestion, and fatigue

36. Women and Acute MI What causes atypical presentations?
Anatomical factors
Physiological factors
Pathological factors
The above list may demonstrate the causes of the differences between males and females in typical versus atypical presentation of acute MI

37. Atypical Presentations of Elderly
Most likely complaints
Dyspnea
Diaphoresis
Nausea
Syncope
May have atypical presentation most likely due to altered pain perceptions

38. Atypical Presentation of Long Standing Diabetes
Silent ischemia considered due to autonomic denervation of heart
Nerve damage that disrupts signals between the brain and other body parts
Diabetics recognized at risk for atherosclerotic plaque formation and thrombosis contributing to acute MI

39. Diagnosing Cardiac Problems
Patient history of events
12 lead EKG analysis – changes over hours & days
Large peaked T waves, then ST elevation, then negative T waves, then pathological Q wave development
Cardiac markers – blood work
Timing of the rise and fall of enzymes can help predict when the acute process occurred
Troponin I levels
Specific to myocardial damage

40. Cardiac Markers

41. Have you ever wondered…
What will I see on the EKG if the patient is having angina and not an MI?
ST elevation can occur (rarely) if perfusion is poor or some spasm is present; it could take some time for the ischemia to normalize
When ST elevation on EKG is from a paced rhythm or LBBB, how do you decide when to take the patient to the cath lab?
Most often history and how the patient looks are deciding factors. Cardiologists would rather find normal arteries than miss an MI. Comparison with old EKG’s could help if they are available

42. Questions cont’d….
If the patient is having atypical angina attacks, what is the likelihood that they will have an acute MI?
This is very predictive with a rate of at least 30% within 30 days
Do all persons with an MI develop a diagnostic Q wave that shows on the EKG forever?
Diagnostic Q waves do not develop immediately and may not if response and repair is rapid. They depend on the thickness of the infarct and length of time before treatment

43. Delay in Seeking Care
Atypical presentations (absence of chest pain) increase the delay before seeking care
TIME IS MUSCLE!!!
Delay in appropriate assessment and intervention increases the mortality rate

44. What Therapies Are Available for Diagnosing and Treating AMI?
Angiogram / Cardiac catherization
Insertion of long flexible tube into artery or vein
Die injected to evaluate blood flow through coronary arteries
Fibrinolytic therapy
Medication used to dissolve the clot

45. Therapies cont’d Angioplasty / PTCA
Percutaneous transluminal coronary angioplasty
Balloon tipped catheter introduced into femoral artery
Advanced to coronary artery
Balloon expanded to press clot into wall of artery
Stent may be left to keep lumen open
“Door-to-balloon” phrase often heard

46. Therapies cont’d CABG / “open heart”
Coronary artery by-pass graft surgery
Small vein removed from the patient (i.e.: leg) and attached to the aorta and then a point beyond and by-passing the blockage

47. Angiogram With Severe LAD Stenosis

48. Stent Placement in LAD

49. LBBB Pattern & Paced Rhythms in Acute MI
Diagnosis difficult based on the EKG
The baseline ST segments and T waves shift masking or mimicking acute MI
Assume acute MI and treat as such
Hospital assessment includes lab analysis and MD assessment
Patients may be taken to the cath lab on presumptions
MD would rather err on side of being aggressive than to be delayed in treatment of acute process

50. LBBB Pattern on 12 Lead EKG

51. Paced Rhythm 12 Lead EKG

52. Region X SOP – Adult ACS Adult Routine Medical Care
Obtain 12 lead EKG and contact Medical Control for STEMI alert if ST elevation noted
Note: contact Medical Control first if ST elevation in II, III, aVF (inferior wall MI) prior to administration of nitroglycerin and morphine
Patient susceptible to episode of hypotension

53. ACS SOP cont’d Determine if patient is stable or unstable
What is the level of consciousness?
What is the blood pressure?
What are the skin parameters?
If unstable, limit medication to aspirin 324 mg chewed, if patient can tolerate
Consider IV/IO fluid challenge in 200 ml increments
Early contact with Medical Control important

54. ACS SOP cont’d If patient is stable Aspirin 324 mg chewed
If chest pain, Nitroglycerin 0.4 mg sl
Screen for MI location, B/P, Viagra-type use previous
May repeat every 5 minutes as needed
Maximum of 3 doses
Manage pain appropriately
Morphine 2 mg IVP over 2 minutes
May repeat every 2 minutes to a maximum total dose of 10 mg

55. Aspirin Extremely important
One of the single most important interventions that reduces morbidity and mortality
Prevents platelet aggregation to site of fractured plaque
Prevents increase in degree of blockage to blood flow
Better to have patient take an extra dose than to totally miss any coverage with aspirin

56. Development of a Stroke
Clots, plaques, & hemorrhage causing problems

57. 2 Main Types of a Stroke Ischemic – the more common (83%)
Blockage of blood flow in a vessel
Thrombotic stroke – blockage by blood clot development in artery supplying brain
Embolic stroke - blood clot from another area of body travels to brain and blocks blood flow
Atrial fib most common cause
Hemorrhagic – more deadly (17% occurrence)
Tearing or rupture of a weakened vessel
Blood spills into or around the brain

58. Pathophysiology of Stroke
Ischemic (blockage) versus hemorrhagic

59. Major Risk Factors for Stroke
Atherosclerosis
High cholesterol levels
Hypertension
Diabetes
Smoking

60. Additional Risk Factors Leading to Stroke
Obesity
Alcohol consumption
Substance abuse – particularly cocaine
Oral contraceptive use
Sickle cell disease
Atrial fibrillation rhythm
Sedentary habits promoting development of deep vein thrombosis (DVT)
Surgery, lengthy travel, immobility due to casting

61. Ischemic Stroke Symptoms
Similar to TIA but damage can be permanent
Dependent on area & size of brain affected
Most common symptom: sudden unilateral weakness face, arm, and/or leg
Sudden confusion, trouble speaking/understanding
Sudden visual changes
Sudden trouble walking, dizziness, loss of balance or coordination

62. Hemorrhagic Stroke Symptoms
Rupture can be from high blood pressure or cerebral aneurysm
Location of hemorrhage, not amount of bleeding, influences severity of stroke
Intracerebral – bleeding within the brain
Hypertension most common cause
Blood vessel abnormalities (AVM, AVF) can cause pressure on tissue or rupture
Subarachnoid hemorrhage
Bleeding between brain and skull
Most common complaint – severe headache!

63. Arteriovenous Malformations - AVM
Masses of arteries and veins without intervening capillaries
Vessels dilate and often twist
Tend to be congenital & near back of brain
High pressured arterial blood flow of arteries empty directly into thin walled veins
Stress can cause rupture of vessel
Exchange of oxygen and nutrients hampered
Normally occurs via system of capillary walls

64. Arteriovenous Fistulas - AVF
Can be congenital but more often caused by trauma that damages an artery and a vein lying side by side in the brain
Artery and vein join together losing the protective separation of capillary system
AVM and AVF problems
Hemorrhage into surrounding tissues
Pressure on adjacent part of brain creating neurological deficits

65. General Treatment AVMs and AVFs
Surgery to tie off or clip arterial vessels that feed the abnormality
Endovascular embolization
Injection of agent to block blood flow through abnormal connection (i.e.: special glue, coil, balloon)
Radiosurgery
External beams of radiation to injure or clog the abnormality – can take weeks/years and can damage surrounding tissue

66. Hospital Diagnosing of a Stroke
Confirm the problem is an acute stroke
Eliminate other possibilities
Determine type of stroke – ischemic or hemorrhagic
3 dimensional imaging (CT scan, MRI) and other specialized testing processes
Determine time of onset, location and severity of stroke
Dictates treatment approach

67. Field Assessment of Possible Stroke
Maintain high index of suspicion!!!
Not all stroke presentations are clear cut!!!
Blood glucose level to rule out other issues
Cincinnati Stroke Scale
Facial droop – right, left, none
Arm drift – right, left, none
Speech – clear, not clear
Did we mention maintain high index of suspicion???

68. Hospital Treatment of Stroke
Goal – remove blockage and restore blood flow
Thrombolytic drug therapy – tPA (clot-buster)
Short window of time to deliver (3-41/2 hours from onset)
 incidence of intracranial bleeding after this time
Mechanical device on end of catheter to pull out all or part of clot
Requires specialized surgery and practitioner
Administer antiplatelet meds (i.e.: aspirin)
Maintain normal blood sugar levels
Abnormal levels can aggravate stroke damage

69. Region X SOP Treatment - Stroke
Adult Routine Medical Care
Determine time of onset of symptoms
Referred to as “last known normal”
Obtain blood glucose level
Treat if level <60
Perform Cincinnati Stroke Scale
Record specific abnormal responses in the narrative
Box provided in Image Trend only allows normal/abnormal comment

70. Stroke SOP cont’d Contact Medical Control
Needs early notification to prepare timely response
If rapid neurological deterioration, ventilate pt
1 breath every 3 seconds
Document 20/minute assisted for respiratory rate
Consider Drug Assisted Intubation if needed

71. Treatment Stages for Stroke
Prevention
Behavior modification & lifestyle changes
Use of anticoagulants/blood thinners
Prevents clot formation or growth; does not dissolve clots already formed
Intervention during acute phase
Intensive care immediately after
Rehabilitation
Physical , occupational, speech, audiology therapies as an in or out patient basis

72. Stroke Outcomes 10% stroke survivors recover almost completely
25% recover with minor impairments
40% recover with moderate to severe impairment
Will require special care
10% will require care in nursing home or other long-term care facility
15% die shortly after the stroke

73. Patient Role in Stroke Care
Recognition of signs and symptoms of a stroke
Important role of the healthcare worker to educate the public on this information
Activating 911 without delay
Minimizing risk factors by adopting healthier life style choices

74. TIME IS BRAIN!!! EMS Role in Stroke Care
Determine general impression keeping high index of suspicion for stroke
Perform appropriate physical exam
Obtain adequate history
Transport to closest appropriate hospital with minimal delay
Providing early report allows receiving facility to be prepared – clock is ticking!
TIME IS BRAIN!!!

75. Obtaining Pre-hospital 12 Lead EKG’s
Many patients will be monitored for their baseline rhythm
Not all patients monitored require a lead EKG
Any 12 lead EKG obtained must be interpreted and transmission attempted to the receiving facility, if capable

76. 12 Lead EKG’s When in doubt, obtain a 12 lead EKG
Silent MI’s do occur
The patient has absolutely no complaints of pain
Any complaints will most likely be very vague
Absence of ST elevation (non-diagnostic EKG) does not mean the patient has no cardiac issue going on
Maintain high level of suspicion based on clinical presentation and history of present illness

77. Case Scenario #1 37 y/o male crushing chest pain over the sternum
Cool/clammy, anxious
VS: B/P 90/58; P – 124; R – 26; SpO2 96%; pain 3/10
EKG monitor attached
Your general impression?
Acute MI until proven otherwise
Differential should include other cardiac problems, respiratory problems, GI problems
ALWAYS go for the worst case scenario!!!

78. Case Scenario #1 – What’s this rhythm?
Sinus tachycardia
What other assessments need to be obtained that help narrow down a general impression?
12 lead EKG
Head-to-toe hands-on assessment especially of cardiac and respiratory systems

79. Case Scenario #1 What interventions have been started?
Vital signs, pulse ox, pain scale
Preparation to obtain 12 lead EKG
Aspirin to chew if no contraindications
Hold nitroglycerin until B/P, 12 lead EKG reviewed and history verified of no Viagra type drug use last
ST elevation in inferior wall (leads II, III, aVF) would prompt restriction of therapies that would trigger vasodilation responses

80. Case Scenario #1 – Reassessment
VS: B/P 100/60; P – 106 irregular; R – 22; SpO2 97% RA; pain 2/10; lungs remain clear
What is the rhythm?
Sinus rhythm with multifocal PVC’s

81. Case Scenario #1 - Reassessment
Do you treat the rhythm?
Monitor for now
FYI: PVC’s common dysrhythmia in COPD & cardiac irritability; they don’t all need to be treated
VS: B/P 106/64; P - 98 reg; R – 22; SpO2 98% RA
VS: B/P 110/70; P – 72 reg; R – 16; SpO2 100% RA; pain 0/10

82. Case Scenario #2
55 y/o female presents with weakness in right arm starting 1 hour ago
Appears shaky and scared; warm and dry
Hx: elevated cholesterol levels, mild hypertension
VS: B/P 160/92; P – 88; R – 18; SpO2 99% RA
What is your general impression and what assessments or interventions would be done?

83. Case Scenario #2 General impression to consider
Acute stroke high on the list
Could be anxiety, slept funny, resting arm in awkward position
Can you rule out stroke based on patient age and absence of risk factors?
NO!
Young children can have strokes
Usually different etiology than older adults

84. Case Scenario #2 Can symptoms predict part of brain affected?
Yes
Frontal lobe – planning, problem solving, personality, higher cognitive functions
Parietal lobes – touch, pressure, fine sensation
Lt parietal – expressive/receptive aphasia
Rt parietal – visuo-spacial deficits
Hard to find way around even familiar surroundings
Temporal lobes – smells and sounds; short term memory
Occipital lobe – processing visual information

85. Case Scenario #3 69 y/o female c/o intermittent SOB several days
Alert, tired looking, lightheaded, increased fatigue, poor appetite, nausea
Hx: Hypertension,  cholesterol, GERD; ½ PPD smoker x20 yrs (has quit)
VS: B/P 170/80; P – 80; R – 16; SpO2 96% RA
Lungs clear; abdomen soft, non-tender

86. Case Scenario #3 What is the rhythm strip? Sinus rhythm with 1 PAC
Would you obtain an EKG?
You should; vague cardiac presentations common in woman and elderly
Sinus rhythm with 1 PAC

87. Case Scenario #3 – EKG Interpretation?
Normal – no ST elevation noted (or ST depression)

88. Case Scenario #3
If an EKG is normal (i.e.: lacks ST elevation), does this mean the patient for sure is not having an acute MI?
No; patient should still be treated for ACS
ASA
NTG if applicable
Morphine if necessary

89. Case Scenario #3 Suddenly, the patient becomes unresponsive
Now what do you do???
Assess the patient; look at the monitor while checking for a pulse
There is no pulse – now what???
Prepare to defibrillate and begin CPR
What’s the rhythm?
Torsades (pulseless VT)

90. Case Scenario #3 What therapies are necessary running this code?
Defibrillation attempts every 2 minutes
Immediate return to CPR with compressions
Epinephrine 1 mg IVP/IO every 3-5 minutes
Alternate Epi with Amiodarone
300 mg IVP/IO first dose
150 mg IVP/IO repeated dose

91. Common Therapies to Prevent Future AMI
Anti-platelet therapy
Aspirin and/or Plavix
Beta-blocker
Decrease workload of heart
Meds end in “olol”
ACE-inhibitors
 development of heart failure
Meds end in “pril”
Statin therapy
To lower LDL levels of cholesterol

92. Case Scenario #4
78 y/o male presents with weakness and dizziness; complains of inability to get out of bed
Hx: Hypertension, gout, diabetes, MI x2 with hx CABG 3 years ago
Alert and oriented; responding to all questions
VS: B/P 172/86; P – 150 irregular; R – 20; SpO2 96% RA; denies pain; lungs clear
What is your general impression?

93. Case Scenario #4 General impression? Could be anything and nothing
Effects of feeling “under the weather”
Stroke
Silent MI
Dehydration
Natural aging process
Could be anything and nothing

94. Case Scenario #4 What’s the rhythm?
What are the risks to this patient?
Atrial fibrillation causing a stroke from emboli in atria
Rapid atrial fibrillation

95. Case Scenario #4 Atherosclerosis High cholesterol levels Hypertension
What are the greatest risk factors for stroke?
Atherosclerosis
High cholesterol levels
Hypertension
Diabetes
Smoking

96. Case Scenario #4
If this were a stroke, what are the important points of assessment & care for EMS to provide?
Assessment
Time of last known normal
Blood sugar level
Cincinnati Stroke Scale
Interventions
Rapid identification and rapid transport
Early report called to receiving facility
Monitor the rapid heart rate – no interventions for now

97. Medication Preparation for Pediatric Patients
CE for September will be running a code for the pediatric patient
In preparation, review math calculations for the pediatric patient this month
Practice reading the SOP’s for orders, following the pediatric medication charts in the SOP’s, and comparing information with the Broselow tape

98. Pediatric Medication Calculation
Determine the proper dosing for the following situations
Be prepared to draw up different volumes of pediatric doses
Compare answers listed in the SOPs with those listed on the Broselow tape

99. Check the SOP’s and Broselow for dosing and compare answers:
Amiodarone for 55#
Versed for 80#
Fentanyl for 60#
Glucagon for 65 #
Narcan for 90#
Valium for 35#
Epinephrine 1:10,000 for 40#
Zofran for 30#

100. Pediatric Medication Calculation
Region X SOP
Broselow Tape
Amio 24 kg – 2.4ml/120mg
Versed 36kg – 0.72ml/3.6mg
Fentanyl 26kg – 0.26ml/13mcg
Glucagon 28kg – 1ml/1mg
Narcan 40kg – 2ml/2mg
Valium 16kg – 0.64ml/3.2mg
Epi 1:10,000 18kg – 1.8ml/0.18mg
Zofran 12 kg – 0.6ml/1.2mg
Amio – orange – 130mg
Midazolam – green - 10mg
Fentanyl–orange–80 mcg
Glucagon – orange - 1mg
Naloxone –up to 36 kg
Diazepam – white - 3.3mg
Epi1:10,000-white- 1.7ml/0.17mg
Zofran-yellow-not listed

101. Pediatric Medication Calculation
Why the difference in dosing from the Region X SOP’s and Broselow tape?
Each group may use a different formula for the medication
Often medication dosing is provided in ranges
Example: 1 – 3 mg/kg
Reminder: Region X SOP – go to the next lowest/closest weight listed in charts
Can always give more if needed

102. Region X SOP Resource vs Broselow Tape
Region X SOP provides “ml” for filling the syringe AND “mg” for documentation
Broselow tape often provides only “mg”
Still need to calculate the “ml” to fill the syringe
Region X SOP medication charts list trade and generic names
Broselow tape often uses only 1 medication name (i.e.: Diazepam, Naloxone, Midazolam, crystalloid fluids

103. Preceptor Role
Provides a guide to transition and integration into the workforce
Supports development of clinical competence and confidence for growth of a professional healthcare provider
Sharing skills and knowledge assures the development of others to continue to provide superior care in an increasingly complex care environment
Must be supported by all in the workplace

104. Bibliography
Bledsoe, B., Porter, R., Cherry, R. Paramedic Care Principles & Practices, 4th edition. Brady
Mistovich, J., Karren, K. Prehospital Emergency Care 9th Edition. Brady
Region X SOP’s; IDPH Approved April 10, 2014.
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diagram-of-the-human-heart-here-are-a-bunch/

105. Bibliography cont’d
cal-reference/myocardial-infarction---by-cornelia-riedl
seasemanagement/cardiology/complications-of-acute- myocardial-infarction/
mike.blogspot.com/2012_10_01_archive.html