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Angina, Acute MI, & Acute Stroke
August 2014 CECondell Medical Center EMS System
Prepared by: Sharon Hopkins, RN, EMT-P, BSN
Rev 8.18.14
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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.
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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.
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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
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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
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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
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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
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Diagram of the Heart
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What is Acute Coronary Syndrome (ACS)?
A list of diagnoses that affect the cardiac system
Indicates an interruption of blood flow to the heartUnstable anginaNon-ST elevation MIST elevation MI
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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
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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!
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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
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Pathophysiology of Angina
Plaque formation
Angina serves as a warning that something is going on
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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
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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
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Variant Angina
Occurs when vessel is in spasm Very painful Often occurs at night Controlled with medication
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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
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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!
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Development of Blockage 19
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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
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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
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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
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Collateral Circulation
Protective mechanism to provide alternative path for blood flow in case of system blockage
Takes time to develop
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Coronary Arteries
Left coronary artery Left ventricle Interventricular septum Part of right ventricle Heart’s conduction system
2 branches Anterior descending artery (LAD) Circumflex artery
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Coronary Arteries cont’d
Right coronary artery Portion right atrium, right ventricle, and
part of conduction system 2 branches
posterior descending artery Marginal artery
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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
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Elements of AMI
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Myocardium and Vessel Structure
Notice that coronary arteries lie on epicardial surface
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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
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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
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Differential Diagnosis…What Could This Be???
Stable angina Acute pericarditis Aortic dissection Pulmonary embolism Pneumonia Pneumothorax
Esophageal spasm Reflux Gastritis Cholecystitis Pancreatitis Musculoskeletal pain
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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)
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Typical Patterns of Chest Pain
May be from surge of catecholamines in response to pain and hemodynamic abnormalities from cardiac dysfunction
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Atypical Presentations
Women, elderly, long standing diabeticsBack painJaw painRight arm painIndigestionNauseaFatigue/weaknessDyspnea/ shortness of breathNo pain
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Atypical Presentation in Women35
Most frequent complaints in women are shortness of breath, weakness, feeling of indigestion, and fatigue
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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
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Atypical Presentations of Elderly
Most likely complaints Dyspnea Diaphoresis Nausea Syncope
May have atypical presentation most likely due to altered pain perceptions
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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
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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
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Cardiac Markers40
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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
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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
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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
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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
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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
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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
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Angiogram With Severe LAD Stenosis47
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Stent Placement in LAD
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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
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LBBB Pattern on 12 Lead EKG50
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Paced Rhythm 12 Lead EKG51
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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
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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
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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 24-480
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
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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
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Development of a Stroke
Clots, plaques, & hemorrhage causing problems
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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
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Pathophysiology of Stroke
Ischemic (blockage) versus hemorrhagic
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Major Risk Factors for Stroke
AtherosclerosisHigh cholesterol levelsHypertensionDiabetesSmoking
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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
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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
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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!
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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
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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
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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
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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
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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???
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Hospital Treatment of Stroke
Goal – remove blockage and restore blood flowThrombolytic 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
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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
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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
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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
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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
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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
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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!!!
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Obtaining Pre-hospital 12 Lead EKG’s
Many patients will be monitored for their baseline rhythm
Not all patients monitored require a 12 lead EKG
Any 12 lead EKG obtained must be interpreted and transmission attempted to the receiving facility, if capable
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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
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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!!!
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Case Scenario #1 – What’s this rhythm?
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
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Sinus tachycardia
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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 24-480 ST elevation in inferior wall (leads II, III, aVF) would
prompt restriction of therapies that would trigger vasodilation responses
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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?
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Sinus rhythm with multifocal PVC’s
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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
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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?
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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
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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
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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
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Case Scenario #3
What is the rhythm strip?
Would you obtain an EKG? You should; vague cardiac presentations common in woman
and elderly
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Sinus rhythm with 1 PAC
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Case Scenario #3 – EKG Interpretation?87
Normal – no ST elevation noted (or ST depression)
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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
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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
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What’s the rhythm? Torsades (pulseless VT)
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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
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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
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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?
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Case Scenario #4
General impression? Effects of feeling “under the weather” Stroke Silent MI Dehydration Natural aging process
Could be anything and nothing
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Case Scenario #4
What’s the rhythm?
What are the risks to this patient? Atrial fibrillation causing a stroke from emboli in atria
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Rapid atrial fibrillation
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Case Scenario #4
What are the greatest risk factors for stroke? Atherosclerosis High cholesterol levels Hypertension Diabetes Smoking
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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
InterventionsRapid identification and rapid transport
Early report called to receiving facility
Monitor the rapid heart rate – no interventions for now
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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
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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
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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#
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Pediatric Medication Calculation
Region X SOP
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
Broselow Tape
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
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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
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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
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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
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Bibliography Bledsoe, B., Porter, R., Cherry, R. Paramedic Care
Principles & Practices, 4th edition. Brady. 2013. Mistovich, J., Karren, K. Prehospital Emergency Care
9th Edition. Brady. 2010. Region X SOP’s; IDPH Approved April 10, 2014. http://www.merckmanuals.com/professional/
neurologic_disorders/spinal_cord_disorders/overview_of_spinal_cord_disorders.html
http://lifeinthefastlane.com/ecg-library/basics/left-bundle-branch-block/
http://www.interactive-biology.com/75/show-me-a-diagram-of-the-human-heart-here-are-a-bunch/
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Bibliography cont’d
https://sites.google.com/site/caduceusnewsletter/medical-reference/myocardial-infarction---by-cornelia-riedl
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/complications-of-acute-myocardial-infarction/
http://www.uhnj.org/stroke/types.htm http://floatnurse-mike.blogspot.com/
2012_10_01_archive.html
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