7220 Acute Coronary Syndrome Flashcards
what is the main problem in ACS?
- reduced O2 supply due to atherosclerotic narrowing of coronary arteries
- inflammatory or vasospastic - Blood flow decreases = symptom of lack of O2
**vasospasm, inflammation and atherosclerosis
Function of the endothelium? 5
- Role of endothelial NO sinthase (eNOS)- nitric oxide synthase enzyme. Dilates. normal levels = can vasodilate coronary arteries. if there isnt then = narrowing***
- sellective barrier between vessel lumen and surrounding tissue
- Regulation of vascular tone and growth
- Regulation of thrombosis and fibrinolysis
- plays a role in immune and inflammatory reactions
causes of endothelial injury: 4
- elevated levels of cholesterol and triglycerides = plaques
- HTN - constant pressure
- smoking
- bacterial/viral infections (flu, strep, pneumocc, RSV)
risk factors to endothelium dysfunction: obese, elevated CRP, chronic systemic infection
what is shear stress?
not laminar
where there are curves, or turbulant flow.
what does shear stress cause?:
- decreased eNOS
- decreased endothelial repair
- decreased alignment/direction of flow
- increased reactive O2 species
- increased leukocyte adhesion
- increased lipoprotein permeability
- increased inflammation
ACS:
Ischemia, injury, infarct
timing and ST/Q-wave
Ischemia- 10-20 min (unstable angina)
ST depress
Injury - > 20 min NSTEMI/ non Q-wave
ST depress
Infarct- > 30 min STEMI/ Q-wave
why might there be refered pain of angina/chest pain?
the same chemoreceptors/mechanoreceptors from the myocardial stretch. Dermatomes are shared to the brain
Classic S and S of angina/chest pain
classic: sweating, nausea, lightheadedness, SOB, plus referred pain
chest pain reflects = end organ perfusion CVS!!!* decreased coronary supply***
Common- silent or nonpainful
Atypical- fatigue or unwell (women, elderly and DM’s)
other: tachy, S3/S4, cardiac/femoral bruit, deficits in periph pulses, HTN, Pallor, Cold Clammy skin, Xanthomas
**pain with exercise that is relieved with rest. HX risk factor
Primary Assess:
NOPQRST
N- normal baseline before onset O- onset time started P- precipitating- how started. Palliative- how it ended Q- quality R- region and radiation S- severity T- timing- how long it lasts
What does the RCA supply?
conduction?
Right coronary artery: Supply: - Right atrium - right vent - inferior and posterior wall of left vent
Conduction:
- SA node 55%
- AV node 90%
- proximal portion of bundle of his
What does the LAD supply?
conduction?
Left anterior descending:
Supply:
- portions of the anterior left and right ventricles
- interventricular septum
Conduction:
- bundle branches (vnet conducting tissue)
What does the Circumflex supply?
conduction?
Supply:
- Left atrium
- posterior/lateral wall of left vent
Conduction:
- SA node 45%
- AV node 10-15%
what happens if you block the RCA?
bradycardia
- evaluation of the right ventricular wall involvement
- some hemodynamic changes
- Potential for significant dysrhythmias caused by SA and AV node dysfunction
- CHF
- cardiogenic shock
what happens if you block the LAD?
- Left vent dysfunction
- potential for hemodynamic compromise
- HF
- pulm edema
- cardiogenic shock
- intraventricular conduction disturbances
what happens if you block the circ?
- evaluation of posterior and lateral wall involvement
- some hemodynamic changes
- dysrhythmias caused by SA and AV node dysfunction
Anteroseptal ECG evidence
V1-V4
Q-waves and ST segment elevation
Lateral Wall ECG evidence
I, aVL, V5-V6
Q-waves and ST segment elevation
Posterior Wall ECG evidence
- V1-V2
- Tall upright R waves with ST depression
- Q-wave and ST elevation in
Inferior Wall ECG evidence
Q-wave and ST elevation in II, III, aVF
Right Ventricle Wall ECG evidence
Q-waves and ST elevations in Right precardial leads RV1-RV6
What is NSTEMI? what happens to the ST? Biomarkers?
No ST elevation or ST depression (ischemia).
cells can be saved if reperfused early
Can have + biomarkers
What does T-wave flattened or inversion mean?
ischemia or resolution phase
What does tall T-waves mean?
Tombstone T waves = early signs of infarction
what does ST elevation mean?
injury.
Cells may recover
what does a Right BBB look like?
where do you see it on an ECG?
rabbit ears
V1-3
What does a left BBB look like?
Where do you see it on an ECG?
top hat
I, V5-6
what happens to the QRS in BBB’s?
it is wide (prolonged)
> 0.12
what are the 3 main evolutionary stages of MI?
- Acute injury
- Necrosis
- Resolution
stage 1 Acute injury…
time between the acute blockage and the tissue death
ST elevation
stage 2 Necrosis…
“dead zone” presence of tissue death
pathological Q-waves
> than one small box or 1/3 the height of the QRS
necrotic cells dies from lack of O2 in blood
Cardiac biomarkers
stage 3 Resolution…
2 weeks after stage 2 scar tissue develops in the infarcted area
persistent Q-waves or inverted T waves*
No cardiac biomarkers
what kind of STEMI do you call this…
Elevated ST in… II, III, aVF
Inferior wall STEMI
RCA
what kind of STEMI do you call this…
Elevated ST in… V1 and V2
Septal STEMI
LAD
what kind of STEMI do you call this…
Elevated ST in… V3 and V4
anterior wall STEMI
LAD
what kind of STEMI do you call this…
Elevated ST in… I, aVL, V5 and V6
Lateral wall STEMI
Circumflex
what is the reciprocal of inferior?
anterior
V1-4
what is the reciprocal of lateral?
inferior
II, III, aVF
what is the reciprocal of anterior?
inferior
II, III, aVF
what is the reciprocal of Anteriolateral wall?
Inferior
II, III, aVF
If you have an ST elevation in V1-V4 then you will have reciprocal in?
Inferior II, III or aVF (at least 2)
When is ST depression significant on an ECG?
When there is no ST elevation**
what do you call paced rhythms
Vent paced, atrial paced or dual paced rhythm
What is ST fingerprinting?
ex. Primary lead II
secondary V2
If the PT has a hx of having an inferior MI are these the best leads to display?
you have primary and secondary lead II and V2
fingerprinting is customizing to display on monitor.
** you would want one of the leads to then be looking at the inferior wall**
if you have a lateral wall MI, what would you want to display on the monitor?
one of I, aVL, V5-V6
Why do we ask you to do
QT analysis
R on T phenomenon
can cause fatal dysrhythmia
QTc
corrected measurement of
which drug prolongs QT or QTc?
Amiodarone
Antiphychotic- haldol, zofran, gravol
whats the best way to document a prolonged QT?
Request for a 12 lead ECG to see if the QT is prolonging. Get a 12 lead to compare to the first one taken
how often do you look at trops?
Q4-6 hrs
stop when the trend starts to go down
whats the diff btwn CK and CK-MB
Creatinine Kinase
CK- non specific substance that would be elevated in ANY event in muscle injury
CK-MB- isoenzyme specific to heart muscles
why do we order these labs: in context of ACS
- HGB, HCT
- Differential count
- Plt
- lytes- which ones
- PT and aPTT
- Glucose
- kidney function
- HGB, HCT- blood flow/ transport. For O2 to body. HCT to see if blood flow is viscus
- Differential count- signs of infection = increased myocardial O2 demand. percentage of blood cells
- Plt- bleeding
- lytes- K+, Ca+, Mg- for myocardial contractility
- PT and aPTT- heparin. need baseline if we want to start hep inf. Mostly with NSTEMI
- Glucose- control for long term management of ACS
- kidney function- for drugs you will give (lasix, ACE inhibit* post-recovery, ARBs, non-steroidal)
We have a PT who presents with chest pain, has risks but has a normal ECG
what to do?
- follow ACS pathway and request cardiac biomarkers. We need to know if it is unstable angina or NSTEMI.
If there are no biomarkers, we can call it unstable angina. if there are biomarkers we can call it NSTEMI
what other diagnostic tests could be ordered?
- CXR- size of heart, lungs
- PET,
- ECHO 2D- EF, vent function, valves (looks like US)
- Coronary angio- artery function
- MRI
- exercise stress test- resolution phase
Treat ACS to avoid complications of MI: 5
- Cardiogenic shock (rapid thready pulse, dyspnea, tachypnea, crackles, +JVD, oliguria, LOC changes)
- Mechanical complications- (vent/septal wall rupture or LV free wall rupture)
- Pericarditis- inflammation
- Thromboembolic Complications- DVT, PE’s, systemic emboli
- Electrical Complications- dysrhythmias, brady/tachy/SVT, other conduction disturbances
What do we give PTs with ACS symptoms?
Imbalance of myocardial O2 supply and demand
MONA
Nitrates
ASA
O2/IV access/12 lead ECG
Morphine (analgesics)
Do you always give the PT O2?
No only if it is under < 94%
Why do we give nitroglycerine ***
- vasodilates coronary arteries to improve perfusion***
2. VENODILATORS= increase venous capacitance vessels = preload will decrease (decrease venous return)
Side effect of Nitro
decrease BP
What can PTs be started on for the management of UA/NSTEMI? examples
- ASA
- Clopidogel (plavix) or ticlopidine
- IV hep or LMWH
- GP IIb/IIIa antagonist (Gycoprotein inhibitors)
How does ASA, Clopidogel/Ticlopidine, GP IIb/IIIa antagonist function for ACS?
Antiplatelet- disrupts platelet adhesion aggregation
How does IV heparin or LMWH function for ACS?
Disrupts thrombin formaiton by binding with antithrombin III and thrombin to create inactive complexes
Heparin is not there to dissolve the clot but to prevent more from forming
How does ASA work?
Inhibit platelet aggregation to avoid clot formation
How does plavix (clopidogel) or ticagrelor work?
When do you use either?….
platelet inhibitors. Decrease Atherosclerosis
clop- inhibits binding of ATP to platelet receptor = inhibit platelet activation/aggregation - clop can cause brady dysrhythmias
ticagrelor- more rapid onset than plavix
How does BB act? why used in ACS?
decrease HR to decrease myocardial O2 demand
will also decrease the contractility
How do ACEI and ARBS act? why use it for ACS
ACE- pril. prevents the conversion of angiotension I to angiotension II to decrease afterload.
to avoid vent remodeling (will learn this later)
What do you need to consider for myocardial reperfusion therapy?
- Length of time from onset of symptoms
2. Hospital capability
Need to treat PT within first
12 hrs. Start count when they get through the doors of the hosp
Symptom to needle
within 30 min for fibrinolytic therapy if you are not near a cath lab
If they are in RCH how long for PCI therapy?
90 min.
Door to balloon time
the goals for treatment of STEMI for time to reperfusion
90 in for primary PCI and 30 min for fibrinolysis
Absolute contraindications for thrombolytic therapy
- previous hemorrhagic stroke at any time
- ischemic stroke within 3 months except acute ischemic stroke within 3 hrs
- known structural cerebral vascular lesion
- known intercranial neoplasm
- active internal bleeding (not period)
- suspected aortic dissection
- significant closed head or facial trauma within 3 months
Caution/Relative Contraindications
- severe uncontrolled HTN on presentation (SBP >180 or DBP >110)
- Hx of prior ischemic stroke > 3 months, dementia, or known intracranial pathology not covered in contraindications
- current use of anticoagulants in theraputic doses (INR>2-3); known bleeding diathesis
- tramatic or prolonged (>10min) CPR or major sx (3 weeks)
- recent (2-4 weeks) internal bleeding
- non-compressible vascular punctures
- for streptokinase/antistreplase: prior exposure (>5 days ago) or prior allergic reaction to these agents
- actice peptic ulcer disease
- pregnancy
- current use of anticoagulants: the higher the INR, the higher the risk of bleeding
RBBB
> 0.12 QRS
V1-3
Small R-large S- large R
Rabbit ears
LBBB
> 0.12 QRS
V1-2
tiny R (if any)- large downward S (can be rS wave) then joins T wave
which are the fibrin selective agents that are the ‘specific clot busters’ (lysis)
- alteplase
- reteplase
- tenecteplase (TNK)
Non-selective thrombolytic therapy agents
plasminogenolysis and fibrinolysis =
stroptokinase
nursing responsibilities for reperfusion therapy:
- Ensure 2x IV access 20g. then no venipunctures for 24 hrs
- ensure drug circulates systemically
- avoid use of auto BP cuffs
- No shaving and avoid brushing teeth
Post-fibrinolytic therapy what to expect:
- evidence or reperfusion: regression of ST segment to normal
- Self-limiting/ non-sustainable dysrhythmias - PVC’s, brady, H blocks, VT
- Washout: early and marked rise in cardiac biomarkers
- prompt relief of chest pain
- Bleeding: bleeding/bruising at puncture sites, blood from any body openeings, skin changes, LOC changes, changes in VS, Hct
What is PCI?
Percutaneous Intervention
Cardiac catheterization
Diagnostic - gold standard treatment procedure
name 2 common PCI’s
- Angioplasty- single or double vessel disease. Displaces plaque and overstretches the vessel with balloon
- Coronary stents - wire mesh tubes as scafolding
Other: Atherectomy, laser angio, cutting balloon angio, brachytherapy
Nursing post-PCI care
(post-cath lab)
- ongoing assessments
(50% of PTs report chest pain after PCI) sites and periph circulation
- telemetry
- assays for biomarkers
- early sheath removal (ART/groin access removal)
- bedrest (3 hr min) and mobility
supine, flat legs, fowlers ok, compression
signs and symptoms of reperfusion
Washout
- cardiac biomarkers rise then fall
- normalize of ST segments
- non-sustained arrhythmias (asymptomatic)
medication Management of Acute STEMI: 5
- Myocardial Reperfusion Therapy - TNK
- Anticoagulation - Heparin
- Prevention of Dysrhythmia - amiodarone, sotalol, lidocaine
- Glucose control/ - insulin?
- Prevention of Ventricular Remodeling - ACEI and ARBS
Clinical guidlines for management of Acute STEMI anticoagulation:
IV Heparin
also give ASA daily
What drugs are used for the prevention of Dysrhythmias?
- Amiodarone
- Beta-Blockers
class 1 - Na+ channel blockers class 2 Beta blockers class 3 K+ channel blockers class 4 Ca+ channel blockers
tobacco contributes to atherosclerosis by
increases LDL and decreases HDL, promotes vasoconstriction and damage to the epithelium
Dysfunction of the Endothelium produces…
Nitric Oxide (NO dilates). Key leukocyte, platelet inhibitors and vasodilator that help maintain vascular smooth muscle cells in a normal, nonproliferative state. Meaning more vasoconstrictor substances are released. This attracts and retains LDL, which in turn becomes fatty streak (foam cells). These cells continue to release inflammatory substances, which weaken the fibrous cap of the plaque
what does wide QRS mean?
BBB
or ventricular related. When higher pacemaker sites have failed or blocked. (vent escape, vent tachy, vent fib, premature vent contractions)
pathological Q wave
at least 1 small box wide and 25% the height of the R
CK
CK-MB
CK creatinine kinase- enzyme found in heart and skeletal muscle. when muscle is damaged CK is released into blood
CK-MB isoenzyme specific to heart
Trop
Contractile protein specific to cardiac muscle.
BNP
brain natriuretic peptide- protein found in heart when having HF
CRP
When there is inflammation in the body
Differential count
signs of infection = increases myocardial demand
percentage of blood cells (WBC’s)
Lytes
Mg, K+, Ca for cardiac function
Kidney function
for which drugs to give
how do you know if MI is acute and not older
if there are no Q waves then it is not in necrosis or resolution phase
If there are no biomarkers, but there are Q waves then it is older (resolution)
when do you give plavix rather then ticagrelor with TNK?
when the MI is inferior due to the risk of brady
If the PT still has nausea, why do you give more nitro?
because there is still an O2 imbalance. Nitro can vasodilate
there are 4 goals to myocardial reperfusion therapy
- re-establish early patency of the coronary artery
- to increase “salvage” of myocardial tissue
- to preserve left vent function
- to increase survival from MI
what are the 2 reperfusion strategies and how long do you have to start them?
either need to be started within 12 hours of onset
Thrombolytic- 30 min
primary PCI- 90 min
rescue PCI if fibrinolytic fails should be done within 120 min
absolute contraindications for thrombolytic therapy
- Previous stroke at any time
- Ischemic stroke within 3 months except within 3 hours
- knows structural vascular lesion
- active internal bleeding
- suspected aortic dissection
- signif closed head injury or facial trauma within 3 months
- severe uncontrolled HTN SBP >180, DBP> 110
avoid automated BP cuffs and brushing teeth, no venipunctures within 24 hrs after heparin stops
2 examples of PCI
- coronary artery angioplasty
2. Stents
how do you know if you have successful thrombolysis therapy?
- reduced chest pain
- reperfusion dysrhythmias (vent premature contractions, vent tachy, accelerated idiovent rhythm, A.fib, vent fib)
- resolution of ST elevation
- abrupt and early rise of biomarkers
what does vomiting induce?
vagal stimulation of SA and AV node triggers parasympathetic stimulation of nervous system to decrease HR and conductivity through the AV node
can worsen bradycardia
what is atropine used for
a vagolytic for bradycardia with AV block
special considerations for PCI
- the stiff wire can perf causing cardiac tamponade
2. the wire can be irritating and cause dysrhythmias
what is loss of capture>
when the pacemaker fires but doesnt create depolarization
