Myocardial Infarction (+ Sudden Cardiac Death) Flashcards
What is a myocardial infarction - MI?
Heart attack: blockage of blood flow to the heart muscle; sustained ischemia (reduced blood flow) leading to IRREVERSIBLE myocardial death or necrosis (cell death)
**80% are because of blood clots
CAD
Coronary Artery Disease
What is ATHEROSCLEROSIS?
disease of arteries because of a collection of plaques OR fatty materials on inner walls of those arteries
What can ATHEROSCLEROSIS be made of?
- fatty streaks
- fibrous plaque
- lesions
What are some risk factors for CAD; and ultimately MI that are NOT MODIFIBLE…
- increased age
- certain ethnicities: white & black
- increased risk for men than women in ages under 75
- genetics
- family hx
What are some risk factors for CAD; and ultimately MI that ARE MODIFIBLE….
- smoking
- obesity
- diabetes (type 2)
- physical activity (limited - little)
- HTN
- lipid profile (increased lipids)
- metabolic syndromes
What does CAD prevention look like?
**identify patients that are HIGH RISK + offer early management of those modifiable factors to allow for early management of CAD for these patients
CARDIAC DIET
- balanced calories
- monitor weight throughout
- smaller meals + more often
- **WHOLE GRAINS + ***HIGH FIBER
- **MORE FRUITS + ***MORE VEGETABLES
- NO sodas, sugary drinks
- **LEAN MEATS
- **SKIM DAIRY
- moderate alcohol intake
- **LOW SALT (2400mg/daily OR less)
- NO deep fried OR limited; bake, broil, grill
- **FISH-OMEGA 3 FATTY ACIDS
What is ANGINA?
ischemia (reduced blood flow) causing chest pain;
this is caused by the narrowing of coronary arteries which leads to MYOCARDIUM HYPOXIA (decreased oxygen to cardiac muscles, increased lactic acid) = PAIN;
**can be acute OR chronic
How can pain ANGINA pain present?
- chest
- sternum
- neck/jaw
- shoulder/arm
- mid-back
- *Can radiate from any location to any other location
Why does an MI have such serious effect on the heart?
ALL heart muscle BELOW the blockage becomes ischemic/necrotic because of LACK OF OXYGENATED BLOOD FLOW reaching that heart muscle; blockage can be complete or even incomplete; incomplete blockages restrict enough blood flow that over time the muscle still dies
Ischemia/Necrotic time frame:
**cardiac cells become ischemic 20 minutes BEFORE cell death occurs (once dead = always dead) YOU CANNOT REVERSE THIS: 30 minutes into ischemic attack, the WHOLE HEART BECOMES NECROTIC/DEAD!!!!!!!
MI Locations: RT Coronary Artery - RCA
- occlusions lead to heart blocks
- **this artery feeds the POSTERIOR part of the heart
- only MASSIVE infarction of RCA = cardiogenic shock
MI Locations: LT Main Coronary Artery - Left Main
**VERY THIN, TINY and QUICKLY leads to sudden death > Widow Maker
MI Locations: LT Anterior Descending - LAD
- leads to LT sided heart failure
* **BIG DEAL because EVERYTHING below becomes necrotic > FULL DEATH of HEART
MI + EKG: what type of EKG is gold standard for MI?
****12 LEAD EKG is ONLY EKG used to determine MI
EKG zones
EKG reads will fall into THREE-ZONES; these zones show what the heart is OR isn’t doing & gives some insight as to what is going on + how severe.
- Zone of Ischemia
- Zone of Injury
- Zone of Necrosis
ZONE OF ISCHEMIA
-ST segment depression (because of lack of oxygen)
»electrical disturbance
***WORK TO RESTORE BLOODFLOW QUICKLY; there is the ability for this area to return to normal without becoming necrotic
-needs follow up but isn’t sudden death.
**ST segment depression MUST be present for AT least 1mm LOW on EKG strip
ZONE OF INJURY
(cells are NOT fully repolarizing because of the lack of oxygen)
- INTERVENTIONS NEED TO OCCUR
- **TREAT EFFECTIVELY & QUICKLY to prevent permanent damage!!!
**ST segment elevation must be present in TWO LEADS; for AT LEAST 1mm HIGH on EKG strip
ZONE OF NECROSIS
(ST elevation = most important part of this on EKG)
-this is where scarring starts to occur; scarring can interfere with muscle function (scarring interferes with ability to conduct electrical impulses)
***Scarring > remodeling; remodeling = increased risk of death
MI zones severity: least > most
ZONE OF ISCHEMIA > ZONE OF INJURY >
ZONE OF NECROSIS
What do you want to prevent in an MI, which can ultimately be life saving!?
***preventing REMODELING is very important and can safe your patients life!
STEMI vs NSTEMI
STEMI = ST(segment) ELEVATED MI
^^^^^^**EMERGENT
NSTEMI = NON ST(segment) ELEVATED MI
^^^^^^***NON-EMERGENT but requires follow-up!
STEMI (ST(segment) ELEVATED MI)
***MUST be determined by 12 lead EKG + MUST show up on 2 of the leads @ 1mm HIGH
> > Intervention needed IMMEDIATELY; could mean coronary artery is occluded > heart muscle death likely
NSTEMI (NON ST(segment) ELEVATED MI)
-likely from an INCOMPLETE coronary artery occlusion
**chest pain likely present BUT oxygen + nutrients are still being supplied
-needs treatment/attention BUT is not emergent
»>no Q wave will be present
Main goals for a patient with possible/likely/identified MI
- minimize damage
- preserve function
- reperfusion of myocardial muscles
- prevention of complications
How can I prioritize my care as a nurse to achieve these goals?
#1: Assess ABC's: airway, breathing, circulation #2: Position for optimal gas exchange + admin oxygen #3: Obtain vital signs #4: 12 Lead EKG #5: IV access #6: Assess pain using (PQRST) #7a: Admin NITRO #7b: Admin aspirin #8: Admin morphine #9: Continuous EKG monitoring #10: Obtain bloodwork #11: Chest X-Ray #12: Admin STATINS
1: ABC’s
Airway
Breathing
Circulation
2: Position + Oxygen admin
Ensure your patient is upright
Admin oxygen as/if needed
**O2 goal with MI is 93% or greater
3: Obtain vital signs
Frequently assess vital signs + compare to previously obtained or baseline vital signs to determine any significate changes!
4: 12 Lead EKG
MI CANNOT be dx’d without a 12 lead EKG; this is gold standard for MI dx!
5: IV access
you may/may not need more than one IV access site: you might need to give medications and or fluids and they may not all be compatible with each other!
6: Assess PAIN w/ PQRST
P: precipitating event: what lead up to the MI/chest pain; what were you doing?
Q: quality of pain: how bad is it, what kind of pain is it?
R: radiation of pain: is the pain radiating to other locations?
S: severity of pain: how severe is the pain, what level 0-10, etc.
T: timing: how long has the pain been present?
7a: Administer NITRO
NITRO can be administered Q5minutes for 15 minutes;
nitro will TANK B/P, DO NOT give if patient is HYPOtensive.
- *Assess allergies before admin
- **Assess previous admin before admin: was patient brought in by ambulance and given by EMT? these need to be determined before administration!
7b: Administer Aspirin
Admin Aspirin after NITRO, if needed; normally 325mg chewable tablet
8: Administer Morphine (IV)
IF nitro doesn’t relieve the pain, or achieve desired effect, administer morphine BUT only AFTER NITRO; same considerations for Morphine because morphine can TANK B/P and cause HYPOtension; what is B/P?
9: Continuous EKG monitoring
patients with MI/possible MI are at higher risk for other dysrhythmias **A-FIB; they need to be attached to continuous monitoring to ensure these are addressed if happens
10: Obtain bloodwork
Bloodwork needs to be obtained to see what is going on:
- electrolytes
- CBC
- cardiac markers
11: Chest X-ray
is there any cardiac enlargement? is there anything else on this x-ray that makes you think its NOT an MI? etc.
12: Administer STATINS
Administer HIGH DOSE STATINS
What S/S should I look for in my patient + what S/S should I educate my patient to look for?
***SUDDEN ONSET CHEST PAIN that:
-NOT relieved w/ rest OR medications
-20 minutes or longer
-the chest pain feels CRUSHING (like elephant
sitting on chest, etc.)
-neck/jaw, epigastric, sternal or back pain
**SOB
**nausea
**anxiety
**cool, pale, moist skin (grey in appearance)
**indigestion (not relieved with antiacids)
**INCREASED RR + HR (this is compensatory)
^^^ trying to blow off more CO2 to get more O2
What is so significate about Diabetes and MIs?
**diabetics are KNOWN to have SILENT MIs because of their increased neuropathy (they cannot feel it because of this)
Diabetics and MIs
diabetics NEED:
-continuous monitoring: this helps determine any changes that are occurring since your patient may or may not feel these changes; this also helps know what/when medications are necessary
What else can you do for diabetics regarding MIs or possible MIs?
- offer SUPPORT
- EDUCATE the patient on what to look for
- *prepare for POSSIBLE emergency: crash cart, intubation kit, etc.
What labs/diagnostics are important for determining an MI?
**Troponin **Lipid Profile **Chest X-Ray The GOLD STANDARD lab for MI is: TROPONIN (T)/(I) TROPONIN T: 0.1+ = POSITIVE for MI TROPONIN I: 0.04+ = POSITIVE for MI
What is important to remember about TROPONIN?
TROPONIN elevation occurs 4-6 hours POST-INJURY and can last up to 10-14 days!
What does treatment for NSTEMI patients look like?
1: start on antiplatelet drugs (aspirin/heparin), to prevent clot formation
^^^^increases bleed time; so monitor) #2: start on beta-blockers
^^^^decreases workload on heart #3: start ACE inhibitors/ARBs
^^^^decreases workload on heart + decreases
remodeling #4: start/administer NITRO (vasodilates)
^^^^reduces workload AND pain
What type of treatments are performed in the operating room for MI patients?
- coronary artery bypass graft
- off-pump coronary artery graft
What physiological changes can occur after an MI?
- leucocytes start coming to the heart and start remodeling! (DO NOT WANT)
- necrotic muscle = THIN MUSCLE; which leaves the patient at risk for ventricular aneurysms!!!!
