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

4

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

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

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

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

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

Paced Rhythm 12 Lead EKG51

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

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

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

Case Scenario #3 – EKG Interpretation?87

Normal – no ST elevation noted (or ST depression)

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)

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

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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