Week 3- ACS Flashcards
characteristics of GI pain
burning
cramping
respiratory characteristics of chest pain
sharp
changes with inhalation and exhalation
cardiac characteristics of chest pain
crushing
pressure
three types of chest pain
description
burning
stabbing
pressure
Gi causes of chest pain
GERD
Esophageal
Abnormal motility
Hyperadrenergic status causes of chest pain
5
- stress induced
- cardiomyopathy
- cocaine intoxication
- methamphetamine intoxication
- pheochromocytoma (tumor of adrenal gland)
chest wall causes of chest pain
msk
nerve pain
psychogenic/psychosomatic causes of CP
2
panic disorder
depression
pulmonary causes of CP
PPPPAC
6
PE
pulmonary htn
cor pulmonale
lung parenchyma (pneumonia, cancer)
asthma/COPD
pneumothorax
cardiovascular causes of CP
3
Ischemic:
- CAD
- Vasospasm
- Cardiac syndrome X
Non ischemic
- pericarditis, myocarditis, acute aortic syndromes
Valvular
progression of atherosclerosis
- chronic endothelial injury (damaged endothelium)
- fatty streak (lipids accumulate and migrate into smooth muscle cells
- fibrous plaque (collagen covers the fatty streak, vessel lumen is narrowed, blood flow is reduced, fissures can develop)
- complicated lesion (plaque rupture, thrombus formation, further narrowing or total occlusion of vessel)
Risk factors for atherosclerosis
Smoking
HTN
Diabetes
High cholesterol
Obesity
Fam hx
Age >65
Alcohol/drugs
Diet
inactivity
Stress
VIRCHOWS TRIAD
contributors to a DVT or other clots
1) venous stasis
2) vessel wall damage
3) coagulation
causes of hypercoagulability
M M P I I I I A E D
10
- major surgery
- malignancy
- pregnancy
- inherited thrombophilia
- infection/sepsis
- IBD
- autoimmune condition
- estrogen therapy
- inflammation
- dehydration
causes of vascular damage
7
- thrombophlebitis
- cellulitis
- atherosclerosis
- indwelling catheter / heart valve
- venipuncture
- physical trauma, strain or injury
- microtrauma to vessel wall
causes of circulatory stasis
CLAVVI
- immobility
- venous obtruction
- varicose veins
- a fib or left ventricle dysfunction
- congenital abnormalities, affecting venous anatomy
- low HR and BP
PE caused by
obstruction of the pulmonary artery or one of its branches by a thrombi
PE originates in
3
venous system or RA or RV
risk factors for DVT
HATP
- associated with trauma
- pregnancy
- HF
- > 50
thrombotic and embolic causes of PE
DVT, Afib
fat, amniotic, air
S/S of PE
Depend on the size of thrombus and the area where the occlusion occurs
- Dyspnea
- Tachypnea
- CP sudden onset – pleuritic
- pale
- diaphoretic
- decreased SpO2
- hemoptysis
- panic, anxiety
- tachycardia
hemoptysis
pink frothy sputum
nursing intervention PE
- get help (call bell)
- O2
- Increase fowlers
- call MRP
- ensure working IV
- heparin (PE DVT and cardiac)
MRP orders for suspected DVT
8
- CXR
- CT PE (with contrast dye)
- ABG
- ECG
- coags
- D-dimer
- trops
- C reactive protein (general inflammation)
thromboembolism treatment
Anticoagulants
role of anticoagulants
- don’t actually thin your blood, rather delay clotting time
- goal is to prevent thrombus from growing and fragmenting
- prevent new thrombus formation
unfractionated heparin
whole, standard IV heparin
LMWH
fractionated heparin
- dalteparin, enoxaparin, nadroparin
- great if higher risk of clotting
- great when we don’t want a heavy hitter
fondaparinux use
- given sc
- to act more like a thrombolytic (kind of think about it like an off label use that some drugs have).
- We use either use this stand-alone (usually AFTER we are unable to give TNKase or we can give in conjunction).
- it does not have as much bleeding effects as say a LMWH
warfarin
oral anticoagulant
- a fib
- mechanical heart valves
new oral anticoagulant (NOACs)
examples
uses
apixaban
rivaroxaban
dabigatran
- a fib
dont use for mechanical valves
when would give anticoagulants post op
types of surgery
- ortho surgery
- cardiac surgery (stable waiting for surgery, prevent clot formation)
if someone found to have a fib
will start with IV or subcu and then transferred to an oral to sustain the levels
nursing considerations for anticoagulants
watch for bleeding
check coags before (INR, PTTs, Platelets, hgb)
Factors which may determine peri-op myocardial ischemia and infarction
2
- ↓ myocardial O2 supply
- ↑ myocardial demand
↑ myocardial demand
3 STD
↑ myocardial wall stress
Dysrhythmia
Changes in body temperature
↓ myocardial O2 supply
3
Hypoxia
↓BP (stress will bring it up)
Coronary vasospasm
common non modifiable risk fators
- fam hx
- age
- male
women after menopause
more at risk for cardiac issues
modifiable RF
5
- diet
- HTN
- Activity level
- Stress level
- Alc/drug use (messes with coagulation)
downers vs uppers
resp depression, decrease LOC
uppers: cocaine, meth= stimulant, increase RR, HR, BP will cause stress on body, meth is given for ADHD (as you age make sure get assessed for cardiac functioning)
risk factors for high cholesterol
- high Lp (a)
- High LDL
- Low HDL
LDL
HDL
low density, light and fluffy, (marshmallow sticks everywhere)
<2 mmol: normal person
<1.8 mmol: cardiac issue
dense, will slip down (rock)
>1.03 higher the better
Lp(a)
- newly discovered, target should be less than 100
- Risk of cardiac disease will get the test done once in your life
statins
lower LDL increase HDL
Chest pain that is the result of
myocardial ischemia
types of angina
Stable*
Acute Coronary Syndrome*
Variant (Prinzmetal)
atypical
stable angina
- predictable, have small clots but not fully occluded
- will come on with stress or exercise
- relieved by rest
ACS is a umbrella term for
1- unstable angina
2- NSTEMI
3- STEMI
variant CP
Coronary vasospasm, constriction but not actually caused by a clot. Doesn’t follow MI type of pain
unstable angina
5
Narrowing and worsening
No longer responds to rest
Wake up in middle of the night
No platelet aggregation
Small thrombus formation
NSTEMI
- Both thrombus and platelet aggregation
- Large coronary artery we do not get complete blockage
- Incomplete blockage of the large coronary arteries
- Can also see a complete blockage but in small coronary arteries
- Will not elevate ST segment
STEMI
Full occlusion of the coronary artery
Platelet has covered artery
0 blood flow
3 main coronary arteries
LAD
Left circumflex
Right coronary artery
LAD and left circumflex come off left main.
woman and people with diabetes
3
- diffuse epigastric pain
- flu like symptoms
- nausea
coronary bridging
Coronary arteries are on top of heart
This is when the coronary artery is inside the heart muscle when contracts causes chest pain
COLLATERAL CIRCULATION
Arterial branching
Develops over time in response to chronic ischemia
Rapid onset CAD no time to develop collateral circulation
query MI what to do next
Quick bedside 12 lead ECG (#1)
Cardiac enzymes
*troponin (most specific)
- CKMB (heart muscle)
- Myoglobin (general muscles)
leads are
different views of the heart
ST elevation=
myocardium does not have enough oxygen, getting shift in electrical conduction
ECG=
electrical conduction of the heart, any kind of movement in the muscle we need electrical conduction
ECG
usually resting
12 lead most common
left ventricle
rate, rhythm, st elevation or not
P wave:
QRS complex:
T wave:
Atrial relaxation
- atrial depolarization (contracting)
- ventricular depolarization (ventricles bigger so longer)
- ventricular repolarization (ventricles relaxing)
- is happening behind the ventricle contracting
ST elevation
YES=
NO=
algorythms
YES= STEMI
NO then look if
cardiac markers raised
no= unstable angina
Yes= NSTEMI
cardiac enzymes
CK
CKMB
troponin
CKMB
onset
peaks
normalizes
Creatine kinase myoglobin
Onset 2-3h
Peaks 15-24
Normalizes 3 days
troponin
o
p
n
Onset 4-6h
Peaks 10-24h
Normalizes 10-15 days
How do we know when they are done having their heart attack
Serial troponin (looking for a decline, want to know what was the highest mark) are they still having an MI
3 troponins 6 hours apart
What if its still climbing- order another one
Meds for MI
5
- (#1) P2Y12 receptor antagonist – Clopidogrel (Plavix), Ticagrelor (Brilinta)
- (#2) ASA (Aspirin)
- Nitroglycerin Spray
- Beta Blocker
- ACE-I or ARB
when nitro not good
not good if already hypotension, aortic stenosis), look at BP and history
why give BB ACEI and ARBS
reduces contractility and decrease myocardial demand
Mi interventions
depends where you are
- large tertiary hospital
PCI
- smaller hospital determine if enough time to wait for PCI
- Fibrinolytic is no time
CABG
ABSOLUTE Contraindications
of thrombolytics
1. (3)
2. (2)
3.
Brain Problems:
- Intracranial Hemorrhage (ICH)
- Recent ischemic stroke <3months
- Brain CA
Bleeding Problems:
- Aortic Dissection
- Recent (within 3 months) Trauma/Active Bleeding
Uncontrolled Hypertension
RELATIVE Contraindications
thrombolytics
Brain Problems:
- Ischemic stroke > 3months
- Other neuro issues
Bleeding Problems:
- High INR, anticoagulant use
- Recent bleeding
- Traumatic CPR
Controlled Hypertension
primary
rescue
planned
PCI
Primary PCI *
- PCI is the first intervention for the blockage
Rescue PCI *
- PCI is the secondary intervention for the blockage
- Gave clot buster but still some left on the sides
Planned PCI*
- May not have had an acute event but block (ages) are known from a previous Selective Coronary Angiogram (SCA)
