Lecture 3: Coronary Artery Disease and Acute Coronary Syndrome Flashcards
(140 cards)
1
Q
what is the most common cause of hospitalization in Canada
A
CAD
2
Q
When we have someone w irreg rhythm and we are concerned they are deteriorating
A
we can use electricity. Cardioversion uses less, marking. Pacing using a lot less. Defibrillation
3
Q
what happens when we cardiovert a pt if there is a delay from the machine
A
because our heart goes so fast, you wont notice a difference if there’s a delay from machine
we want to avoid over the T wave…???
4
Q
what is CAD
A
- progressive atherosclerotic disorder of coronary arteries
- causes narrowing or complete occlusion of one or more arteries
Stops or decreases blood flow
Stops usually = heart attack
Narrowing = muscle hurts, warning sign, stop progression to heart attack
5
Q
what does Atherosclerosis mean for CAD
A
affects medium sized arteries that perfuse the heart + other major organs. is the progressive build up of plaque in a person’s arteries.
6
Q
describe how CAD can appear (3 ways)
A
- asymptomatic
- stable angina
- acute coronary syndrome
- unstable angina
- MI
- sudden coronary death
*once we have death to cells we cannot do this
7
Q
give examples (9) on what can happen with decreased O2 supply
A
- anemia
- CAD
- hypoxia
- COPD, asthma, pneumonia
- arrhythmias
- CHF
- coronary spasm
- thrombosis
- valve disorders
8
Q
give examples (9) on what can happen with increased O2 demand
A
- anxiety
- cocaine use
- hyperthermia
- hyperthyroidism
- physical exertion
- aortic stenosis
- arrhythmias - increased rate
- cardiomyopathy
- hypertension
9
Q
what in our blood holds oxygen
A
hemoglobin
10
Q
when in the hospital do we usually give blood
A
when hemoglobin is 70 or below or symptomatic usually.
Our bodies have a reserve of O2 for when we exercise and whatnot. So not everyone w a low hemoglobin is at risk.
11
Q
why is taking too much aspirin a risk for anemia
A
People may take too much aspirin for pain, can cause GI bleeds and whatnot, this is a danger because it causes anemia which can cause a heart attack.
12
Q
describe to me about the stages of development in atherosclerosis + treatment
A
Start w lovely vessels, to fatty streak, to fibrous plaque, to complicated lesions. We want to keep peoples arteries open, by interfering and preventing the progression of this disease.
Using pharmaceuticals: cholesterol medications
Diet education: low salt, Mediterranean
Exercise to strengthen CVS - looks different depending on the person.
Treat their comorbidities*** big one like treating HTN, and whatnot.
13
Q
what does the endothelium reguate
A
- dilation and constriction of vessels
- thrombosis - formation of blood clots
- transport of substances to and from vascular space
- growth and ‘apoptosis’ of vascular wall
14
Q
describe endothelial dysfunction
A
- inadequate vasodilation
- prothrombotic
- altered permeability
- increased secretion of growth factors
- increased oxidation of LDL
We can have inadequate dilation - leads to HTN
Form clots we don’t want
Altered permeability - this is important for electrolytes and O2 so we don’t want to affect this
Increase muscle mass - which can be a good thing to a certain degree, but too much makes contraction and availability decreased
Increased O2 of LDLs, promoting the growth of the plaque which is not great
When you vasodilate - causes HTN. Everything in a balance.
Once there is plaque build up to some degree it is reversible, but once 100% occlusion we need to mechanically open those up. - this is last resort
15
Q
whats an angiogram
A
taking a pic of artery and heart to see occlusions. We don’t do this on everyone - but this would be fabulous. Angiogram you usually need to have some type of symptom.
16
Q
describe collateral circulation
picture the picture involving 3 different pictures of plaque building up in the arteries, and how the body maneuvers to solve this issue
A
Bodies always doing things to adapt. Can be good and bad.
Collateral circulation is very good that our body does.
A - what vessels look like - vessels feed the tissue, blood flowing thru
B - as we start to have narrowing, our capillaries start to develop collateral so they start to connect to go around the narrowing. So that there isn’t 100% occlusion. “forms new highways.” someone w a unhealthy diet, doesn’t exercise, and whatnot. Women that are postmenopausal*** our estrogen levels help protect us from this until we are postmenopausal. Women less likely to have collateral develop than men bc of changing hormone levels.
17
Q
hows CAD for women
A
underdiagnosed and common. bc estrogen levels act as a protector until postmenopause.
18
Q
s/s of women CAD
A
more prodromal signs even 2-3 mo prior to actual. Heartburn can mimic heart attack quite regularly.
- absence of cp/or vague
- no radiation of pain
- heaviness of arms
- light-headedness
- epigastric burning
- n/v
- diaphoresis
- feeling flushed
- prodromal symptoms: sleep disturbances, unusual fatigue, SOB, indigestion, anxiety
19
Q
s/s of CAD in males
A
- chest pain/aching/tightness/pressure/jaw pain
- SOB
- pain b/w shoulder blades
- headache
- indigestion
- palpation
- cough
- diaphoresis
- fatigue
- n/v
20
Q
what are challenges of care for CAD
A
- failure to recognize + difficulty interpreting symptoms
- failure of HCP to recognize prodromal symptoms
- ECG and stress test less sensitive
- plaque tends to be distributed diffusely
- less likely to be evaluated for risk factors or treated aggressively
21
Q
describe presentation of CAD in the elderly
A
*atypical
- most frequent s/s of acute MI: SOB, fatigue and weakness, abdominal or epigastric discomfort
- often have preexisting conditions making this an already vulnerable population: HTN, CHF, previous AMI
- likely to delay seeking treatment
22
Q
how would CAD present in a pt with diabetes
A
- atypical presentation due to autonomic dysfunction
- common s/s: generalized weakness, generalized feeling of not being well, syncope, lightheadedness, change in mental status
23
Q
non-modifiable risk factors for CAD
A
- age
- male>female until 65
- genetics
- ethnicity
24
Q
major modifiable risk factors for CAD
A
- tobacco use
- abdominal obesity
- HTN >140-90 mm Hg
- hyperlipidemia
- physical inactivity
25
contributing modifiable risk factors
- psychosocial risk factors (depression, hostility, anger, stress)
- elevated homocysteine levels
- DM
- metabolic syndrome
26
what are low risk factors for CAF (among non-smokers w/o diabetes)
- total cholesterol: 4.7 mmol/L
- untreated bp: <120/<80
should be assessed every 3-5 yr
27
what are moderate risk factors for CAF (among non-smokers w/o diabetes)
- total cholesterol 4.8 to 5.1 mmol/L
- untreated systolic pressure 120-139 mmHg or diastolic pressure 80-89 mmHg
28
what are elevated risk factors for CAF (among non-smokers w/o diabetes)
- total cholesterol 5.2 to 6.1 mmol/L
- untreated systolic blood pressure 140-159 mmHg or diastolic blood pressure 90 to 99 mmHg
should be assessed every yr
29
what are major risk factors for CAD
- treated hyperlipidemia or total cholesterol 6.2 mmol/L
- treated HTN or untreated systolic pressure > or equal to 160 mmHg or diastolic of > or equal to 100 mmHg
- current smoker
- diabetes
30
who should we screen for CAD
- men > or equal to 40 yrs of age, women > or equal to 50 or post-menopausal
anyone with regardless of age: smoker, HTN, elevated cholesterol, diabetic, family history, erectile dysfunction, obesity, inflammatory disease, COPD, HIV
31
pt comes to ER whats the initial assessment if thinking CAD
- baseline VS and 12 lead ECG (within 10 min)
- assessment of chest pain
- associated symptoms
- physical assessment
- medications
if u have time... but if critical can do later
- personal and family history
- environmental factors
- psychosocial history
- pt attitudes and beliefs about health and illness
32
ECG findings within primary assessment
- goal: complete within 10 min of presentation to ER department
- primary diagnostic tool
- changes in QRS complex, ST segment, and T wave
- dynamic process and evolves over time
- repeat every 15-30 min to 2-4 hours
33
for ECG interpretation V2 and V3 look at
is the inferior part (R ventricle, SA node)
34
for ECG interpretation lead 1 and
5 6 look at
is more lateral part of the heart (L atrium, L ventricle)
35
for ECG interpretation V1,2,3,4 and V3 look at
is more anterior part (L ventricle, L atrium)
36
for anterior site on ECG
1. indicative
2. affected coronary
1. V1, V2, V3, V4
2. L anterior descending
37
for lateral site on ECG
1. indicative
2. affected coronary
1. I, aVL, V5-6
2. circumflex or LAD
38
for inferior site on ECG
1. indicative
2. affected coronary
1. II, III, AVF
2. R posterior descending
39
for posterior site on ECG
1. indicative
2. affected coronary
1. reciprocal changes leads V1, V2, V3
2. R posterior descending
40
what causes ST depression
Decrease in o2 delivery
Lack of oxygenation, permanent damage can usually be avoided
41
what causes ST elevation
More than just ischemia, this is injury
Permanent damage is still avoidable but needs to be acted on, time is muscle
Rep of how electricity is going thru the muscle, only way to determine actual damage is doing an echo (ultrasound of heart) to see how it is moving
More aggressive in intervention
42
what does deep and wide Q waves indicate
Deep and wide Q waves = event occurred
Reason we call this dynamic, and continuously do ECGs it can change.
43
OPQRST pain pneumonic
O: onset
P: provocation and palliation
Q: quality
R: region and radiation
S: severity
T: timing
44
common pt complaints or presentations for CAD
- difficulty breathing
- excessive sweating
- unexplained nausea or vomiting
- generalized weakness
- dizziness
- syncope or near-syncope
- palpitations
- isolated arm or jaw pain
- fatigue
- dysrhythmias
45
what are some diagnostic studies for CAD
- 12 lead EKG
- cardiac monitor
- chest xray
- coronary angiography
- exercise stress test
- echocardiogram
46
what is a cardiac angiography used to assess
- coronary arteries
- pressures in cardiac chambers
- valve function
- ventricular function
47
what does the cardiac angiography do
Dye shows blood going thru the arteries
What artery is affected, etc.
They will talk about the occlusion, what should be done about it, etc. (med management)
48
what are stress tests used to diagnose, and what do they do
Put them on a treadmill and make them run
- ischemia, ST segment changes, arrhythmia
- to check functional capacity
- efficacy of medical and surgical intervention
49
what is echocardiography use to assess
- myocardial structures
- ventricular function: ejection fraction, heart motion abnormalities
- effusions
- thrombus
- ischemia
Can see the motion and contraction to see if anything's happening like hypokinesis
See If the valves are snapping shut
See if theirs any regurgitation
See if there's a thrombus and its formation
50
what lab studies are used to assess for CAD
- serum cardiac markers: troponin, serum creatinine kinase (CK), CK-MB
- C-reactive protein
- lipid protein
- blood glucose
- electrolytes
- electrolytes
- kidney function
CK drawn they have to differentiate it - because that’s showing damage to all muscle not just cardiac
CK mb means specifically cardiac muscle
Blood glucose - make sure their levels are fine
Someone w a MI will have better prognosis if glucose is maintained.
Don’t usually take myoglobin
Want kidneys well profuse gotta check those out
51
what is the gold standard for CAD lab studies assessment
troponin
52
how does serum creatinine kinase work
- fractioned into bands - CK-MB
- rises 3-12 hours, peaks in 24 hours
- returns to normal 2-3 days
53
how does troponin work
- 2 subsets cTnT and cTn1
- greater specificity than CK-MB
- levels rise within 3-12 hours
- peak at 24-48 hours
- return to normal over 5-14 days
54
what are some key things to remember about serum cardiac markers
They take a while to elevate in your system (CVS markers)
If it is the beginning of the heart attack it would be normal, takes some time to build up in system of cell death need to trend these
Troponin levels rise within 3-12 hours, peaks 24-48 hrs, returns to normal over 5-14 days
Want to do them again between the 3 hour mark to trend them
55
what pt population most commonly with missed Dx for CAD
- women less than 55 yrs of age
- person of colour
- SOB as major presenting symptom
- normal and non diagnostic ECG (misread)
56
describe the presentation for chronic stable angina
- pain usually lasts 3-5 min - responds well to nitroglycerin
- subsides when the precipitating factor is relieved: physical exertion, temperature extremes, smoking, strong emotions, heavy meal, sexual activity
- pain at rest is unusual
- ECG reveals ST segment depression
- chest pain that occurs intermittently over a long period w the same pattern of onset, duration, intensity of symptoms
- can be controlled w meds on outpt basis
- bc episodes are often predictable, meds can be timed to provide peak effects during the time of day when angina is likely to occur
Responds well to nitro
Patient does something that causes chest pain
Demand increases and cant supply more because of problems
Stop doing the increased demand, then often returns back to baseline - no chest pain
Stents are usually last resort, if not critical will likely do medications for management
57
what are the 4 variants of stable angina
1. silent ischemia
2. nocturnal angina
3. angina decubitus
4. prinzmetal's (variant) angina
58
describe silent ischemia
- ischemia that is asymptomatic
- associated with diabetes
59
describe nocturnal angina
occurs only at night but not necessarily during sleep
if they have this one they wear nitro patch at night vs the day unlike all the other anginas
60
describe angina decubitus
- chest pain that occurs only while lying down
- relieved by standing or sitting
61
describe Prinzmetal's (variant) angina
- occurs at rest usually in response to spasm of major coronary artery
- seen in clients with a history of migraine headaches and Raynaud's phenomenon
- spasm may occur in absence of CAD
- may be relieved by moderate exercise
62
if we have arteries in the heart spasming from angina what do we give them and what does this cause
If we have arteries in heart that are spasming, they are reducing blood flow. Will often give CCBs to prevent spasms from happening.
63
what would unstable angina appear like on assessment
- chest pain that is new onset, occuring at rest or has a worsening pattern
- chronic stable angina that increases in frequency, duration, or severity
- unpredictable, not relieved by rest
- pain refractory to nitroglycerin
- associated with deterioration of once stable atherosclerotic plaque
- unstable lesion can progress to MI or return to stable lesions
- s/s: fatigue, SOB, indigestion, anxiety
Changed or new angina. Doesn’t respond to nitro as much as it used to or changes how it responds.
Is it same or is it different.
64
describe a myocardial infarction
- severe prolonged decreased O2 supply (ischemia) resulting in necrosis
- 90% associated w acute coronary thrombosis
- presence of Q wave - area of necrosis, permanent
- transmural versus subendocardial
65
what to do with an inferior MI (look at diagram on ipad from slides for picture reference)
Do 12 lead ECG
Look for any elevation
Box around 2,3 and AVF
Indicates inferior part of heart there is compromised oxygenation and they are at risk of MI
Want to respond within 10 min of them coming in
If your looking at anterior part, u can see part of posterior but its backwards
We are strictly looking at standard.
So much to look at here.
ECG before nitro.
If we give nitro and reestablish perfusion, then take a pic, it wont look the same. You'd miss the window of diagnoses.
66
what to do with an anterior MI (look at diagram on ipad from slides for picture reference)
Box around anterior leads
V1 looks normal
V2,3,4 we see distinct elevation
So we know there is compromise in O2 delivery to those areas
Anterior MI
Not yet have elevated troponin bc hasn’t been 3 hours yet, but can trend them and do again in 4-6 hours
Having an ST elevation
Need to act accordingly
67
what to do with a lateral MI (look at diagram on ipad from slides for picture reference)
We look at 1, V5, V6
Line does not go to baseline, it is above
Indicative of lateral infarct
If we don’t have full thickness infarct, we may not see elevation. We may just see depression. ST elevation vs non ST elevation MI, these are pts that do not have the classic ECG changes. So if they are having chest pain, but not a classic ECG how do you tell if it’s a ECG - so we have to look at their cardiac enzymes (troponin, etc.)
Unstable angina, or non ST elevation MI - probably have trouble differentiating. If we give them nitro and it resolves then probably angina, but after 3-4 hour if they have elevated CVS enzymes this is non ST elevation MI.
68
describe the zone of infarction of a MI
necrosis and damage
69
describe the zone of injury of a MI
compromise of oxygen delivery but still salvageable
70
describe the zone of ischemia of a MI
still deprived, but salvageable
71
the higher up the damage to an artery...
more muscle it feeds - its what's distal is compromised.
72
for a stemi or non stemi what hour mark will it have elevated troponin
at that 3 hr mark.
73
what does a non ST elevation MI look like on a ECG
Non ST elevation MI - MI that can't be seen on ECG
74
s/s of a MI
- severe immobilizing chest pain that cannot be relieved by rest, position change, or nitrate administration
(diabetic pts may not experience pain)
- epigastric pain - indigestion
-SOB, diaphoresis, n/v
- SNS stim: increased glucose, vasoconstriction (skin ashen, cool or clammy), increased BP and HR (initially)
- CO falls: decreased bp, crackles, JVD, peripheral edema, hepatic engorgement
- pulmonary edema (crackles on lung auscultation)
- dizziness
- extra heart sounds (S3 + S4) - ventricular dysfunction
- fever (systemic manifestation of inflammatory process caused by myocardial cell death)
75
what causes crackles during an MI
R side into pulmonary sys
Pulmonary into L side
Back up of blood into lungs = crackles
76
when jugular veins increase during MI what happens
blood backs up
77
why is hearing S3 S4 not good
S3, S4 (more turbulent, not good, something wrong w the flow of blood)
78
what causes the increased BP and HR initially during a MI
Vasoconstriction = increased BP and HR initially
Don’t restore perfusion to heart - cardiac output falls
79
what 3 things are used for the diagnosis of a MI (2 of 3 criteria required)
1. Chest pain >30min
2. ECG - Q waves/ST segment elevation/T wave inversion
3. Serum cardiac markers: troponin T, creatine kinase (CK)
80
for acute coronary syndrome ischemia....
for stable + unstable angina we have no serum marker release
ecg: ST depression or T wave inversion (unstable angina or NSTEMI)
does not mean cell death so our cardiac enzymes will be normal
ECG could have ST depression with ischemia
81
if we have acute coronary syndrome infarct
we will have a release of enzymes (elevated or positive)
82
for acute coronary syndrome injury: non Q-wave MI
serum marker release
ECG: ST depression or T wave inversion (unstable angina or NSTEMI)
83
for acute coronary syndrome injury: Q-Wave MI
ST elevation (STEMI) with serum marker release
84
STEMI and NSTEMI differences
STEMI
- is en elevation in the ST segment on a ECG
- indicates complete blockage of coronary artery causing more severe form of heart damage
- leads to more extensive damage to the heart muscle + is more life-threatening
NSTEMI
- ST segment does not elevate. Blockage is typically partial not complete
85
Similarity + main difference of STEMI vs NSTEMI
- both involve elevated cardiac enzymes
- can present similarly with symptoms
- ST depression is more a characteristic of NSTEMI, both can potentially show it, but ST elevation is defining feature of STEMI
86
similarities btwn NSTEMI and unstable angina
- present with chest pain, SOB, n/v, sweating, etc
- both can present with ST depression or T-wave inversion on ECG reflecting MI
87
differences in NSTEMI vs Unstable angina
NSTEMI
- elevation of cardiac enzyme
- damage to heart muscle
- more severe
Unstable angina:
- no elevated cardiac enzymes
- heart muscle damage
- no muscle damage
88
goals for pts w ACS
1. relief for ischemic pain
2. effective coping
3. preservation of myocardium (decrease O2 demand, increase O2 supply)
4. immediate + appropriate treatment of ischemia
5. participation in rehab pain
6. reduction of risk factors
We don’t want damage, we want balance
Cardiac death = cardiac dysfunction
89
acute interventions for pts w ACS
- prompt recognition of s/s
- 12 lead and continuous ECG monitoring
- bloodwork (routine, trop, CK-MB)
- oxygenation +/- (keep O2>90%)
- IV access
- initial meds
- immediate reperfusion therapy: PCI or fibrinolytic therapy
90
Initial Medications for MI (4)
1. ASA and Plavix
2. Oxygen
3. Nitro
4. Morphine
91
what is ASA and Plavix for + concentration
- prevent additional platelet activation and interferes w platelet adhesion
- ASA (160-325 mg chewed) and Plavix (600mg)/Ticagrelor (180 mg)
If they haven't taken aspirin they get a loading dose
92
what is oxygen for + concentration
- given to hypoxic pts, resp distress; SaO2<90%
- can worsen size of infarct w high flow rates 8L/min
- titrate to SaO2
93
what is nitro for + concentration
S/L (x3 if needed) followed by IV by persistent pain, hypertension, or heart failure
Nitro we start sublingual
Going to do a bp - If we give nitro sublingually 3x we give them IV nitro
94
what is morphine for + concentration
nitro ineffective; decreased myocardial O2 consumption, decreased BP and HR, decreased contractility
For chest pain we give them morphine - we give nitro first
95
what are additional medication for MI
- B-adrenergic blockers
- LMWH or IV heparin
- Angiotensin converting enzyme
- P2Y12 inhibitors (ticagrelor, Plavix)
- antidysrhythmic meds
- cholesterol lowering meds
- stool softeners
96
what do beta blockers do
lower bp and HR but usually standard
97
what do ACE inhibitors do
reduce bp, reduce constriction, and fluid retention
98
what does low molecular wt heparin
- min after MI, prevents complications
- to prevent re-thrombosis or acute stent thrombosis
99
statin what does it do
low dose, beneficial implications
100
what is mechanical reperfusion
- Primary Percutaneous Coronary Intervention (Primary PCI)
- go in w angiogram
- determine we need stent or not
Mech reperfusion: gold standard - we want our pts to have this promptly, teamed w an angiogram to reestablish perfusion. Can be done emergently, also can be done electively if at risk for an MI
101
pharmacologic reperfusion
1. fibrinolytic therapy
- streptokinase, alteplase (tPA), reteplase (rPA(, tenecteplase (TNK-tPA))
- STEMI only
Fibrinolytic therapy: breaks up clot? To reestablish perfusion
STEMI's ONLY*
If ST are not elevated, even if MD rly thinks so we don’t give fibrinolytic therapy (don’t give to non-stemi's)
Cardiac output = if we don’t have proper cardiac output this is a VERY big problem
102
indications for PCI angioplasty (+/- stenting)
- electively for chronic stable angina
- urgently for unstable angina
- emergently for MI
- 1 or 2 vessel disease
- should be preformed within 120 min for 1st med contact; ideally within 90 min
If its areas we cant reach
Or we cant get to where its blocked because too tiny or hard
Coronary bypass graft - to bypass the blocked area
Someone having a heart attack - we need to get them to Cath lab
Unstable angina - not going to send them home without an angiogram if significant
Ideally within 90
Rurally is more difficult because adding time
103
describe kinda what PCI is + look at the diagram
Eject dye to see where the occlusions are
Once we identify occlusions, we insert the catheter balloon
Going to deflate balloon, and stent and repeat that process
Diagram on L shoes when it is occluded
Diagram on R top shows stent
Because we are accessing a large artery and giving them an anticoagulant = risk for bleeding. Going to have interventions for bleeding.
104
delayed (>120 min) accepted for PCI
- ASA 160 mg PO chew STAT
- Fibrinolytic IV (STEMI only) - in consultation with cardiologist
- Plavix 300 mg PO STAT
- unfractionated heparin bolus 60 unit/kg (maximum 5000 units) is given IV, followed by a continuous heparin drip at 12 units/kg/hr (maximum 1000 units/hr)
- if pts presents w s/s that have lasted longer than 2-3 hrs transfer for PCI
105
immediate accepted for PCI
- ASA 160 mg PO chew STAT
- Plavix 300 mg PO STAT
- Unfractionated Heparin bolus 70 units/kk (max 4000 units)
- standing by for transfer to cath lab
if pts presents w symptoms that have lasted longer than 2-3 hrs transfer for PCI
106
PCI nursing management angina
- may be caused by transient coronary vasospasm, or it may signal a more serious complication
- like restenosis
107
PCI nursing management vascular site care
assessing for bleeding and swelling at sheath site
108
PCI nursing management peripheral ischemia
- secondary to cannulation of vessel, assess for adequate circulation
- looking at distal for good circulation
109
PCI nursing management renal protection
- hydration
- fluids
- D/C of some meds
fluids IV to flush them out, and to have less likely renal toxic complications
If we know they are going to these procedures we can make moves or have orders to prevent the significance of that. Metformin, maybe stop before going to this procedure. Looking at their blood glucose, giving them sliding scale insulin. (if non emergent to be renal protective)
110
what is the target time for fibrinolytic therapy
within first 30 min
ideally within 1st hour after onset of symptoms; less than 6 hrs improved results (mortality rate decreased by 25%)
111
fibrinolytic therapy + dysrhythmias
dysrhythmias are self-limited no tx
112
fibrinolytic therapy + major complication
is bleeding
- surface bleeding - tx. and continue
- major bleed stop infusion
113
fibrinolytic therapy eligibility criteria
- pts w recent onset (less than 12 hours) of chest pain and persistent ST elevation
- pts who present w bundle branch blocks (BBBs) that may obscure ST segment analysis and history suggesting an acute MI
- chest pain unresponsive to sublingual nitroglycerin
- no conditions that might cause a predisposition to hemorrhage
114
sparknotes of fibrinolytic therapy
>120 min
And a STEMI
We could give them fibro lytic therapy.
Time is muscle so within 30 min (within 1st hour super ideal) to break up the clot. Less than 6 hours, they probably won't get this medication.
More than 6 hours -> not much salvaging because a lot of dead muscle - gains are not better than potential risks. Still send them on for a PCI, because don’t have the risk for hemorrhage.
MAJOR COMPLICATION: bleeding. Find if internal bleeding or minor bleeding.
115
absolute contraindications of fibrinolytics therapy
- active internal bleeding or bleeding diathesis (except for menstruation)
- known history of cerebral aneurysm or arteriovenous malformation
- known intracranial neoplasm (primary or metastatic)
- previous cerebral hemorrhage
- ischemic stroke within past 3 mo
- significant closed head or facial trauma within past 3 mo
- suspected aortic dissection
Absolute is something that significantly is 100% increase the likelihood of a major bleed if we give that med
116
relative contraindications of fibrinolytics therapy
- active peptic ulcer disease
- current use of anticoagulants
- pregnancy
- prior ischemic stroke not within past 3 mo; dementia, or known intracranial disease not covered under absolute contraindications
- surgery (including laser eye surgery) or puncture of noncompressible vessel within past 3 wk
- internal bleeding within past 2-4 wk
- serious systemic disease (ex: advanced or terminal cancer, severe liver or kidney disease)
- severe uncontrolled HTN (BP >180/110 mm Hg)
- traumatic or prolonged (>10 min)
cardiopulmonary resuscitation
Relative: assessed on a case by case decision, so pt may or may not receive the medication.
The MD makes these decisions.
117
for chest pain suggesting ACS what's the goal within 10 min
- triage for rapid care
- obtain history
- aspirin 325 mg chewed
- SL nitroglycerin 0.4 mg every 5 min for 3 doses, unless contraindicated
- establish IV access
- obtain blood for initial lab work including serum biomarkers
- institute continuous ECG monitoring
- initiate supplemental O2 therapy
118
if they meet for acute ST elevation MI
give following:
- recommended anticoagulation therapy
- beta blocker if not contraindicated
- IV nitroglycerin if persistent chest pain, unless contraindicated
then...
- primary PCI, if available, w goal less than 90 min OR thrombolysis w goal of 30 min or less
119
if you have a strong suspicion for ischemia, but no persistent ST elevation what do you give
give following:
- recommended anticoagulation therapies
- beta blocker if not contraindicated
- IV nitroglycerin if persistent chest pain, unless contraindicated
120
if you have a strong suspicion for ischemia, but no persistent ST elevation what are you looking for high-risk feature wise
- ST depression
- elevated cardiac biomarkers
- persistent chest pain
- hemodynamic instability
- elevated risk score
121
if you have a strong suspicion for ischemia, but no persistent ST elevation - and have catheterization
catheterization if high-risk features; catheterization or medical management in low-risk pts
122
if pt presents normal or non diagnostic ECG and normal cardiac biomarkers...
- continue elevation and treatment in ED or monitored bed
- repeat ECG and cardiac biomarkers at 6-12 hours
- consider alternative diagnosis
123
if pt presents normal or non diagnostic ECG and normal cardiac biomarkers... and there IS evidence of ischemia/infarction
treat for non-ST elevation ACS
124
if pt presents normal or non diagnostic ECG and normal cardiac biomarkers... and there ISNT evidence of ischemia/infarction
- perform stress test or imaging study
125
what is a coronary artery bypass graft
Go along the vessels and occlude them, and insert into the heart to go around where there is an occlusion to reestablish perfusion distally.
126
who is considered for coronary artery bypass graft (CABG)
- L main disease
- multivessel disease
- satisfactory improvement is not reached w medical management
- pt is not a candidate for PCI (ex: lesions are long or difficult to access)
- lifestyle limiting angina unresponsive to medical therapy or PCI
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what is the ongoing assessment and care post MI s/s to check
- pain
- bleeding/surgical site care, chest tubes, pacer wire care (CABG pts)
- catheter site, assessment of extremities (for PCI pts)
- monitoring: cardiac, resp, VS, O2
- rest and sleep
- anxiety
- effectiveness of interventions
- emotional and behavioural reactions
- evaluation of L ventricular function
- driving - 1 wk post discharge for most pts
- pt teaching
128
long term interventions MI
- BP control
- management of elevated cholesterol
- smoking cessation
- physical activity
- decrease stress - lifestyle
- heart healthy diet
- reduce obesity
- management of DM
- drug therapy
129
HTN management
- having regular BP check-ups
- take prescribed meds for BP control
- reduce salt intake
- never smoke or stop smoking
- control or reduce wt
exercise regularly
130
Elevated serum lipids management
- reduce total fat intake
- reduce animal (saturated) fat intake
- adjust total caloric intake to achieve and maintain ideal body wt
- engage in a regular exercise program
- increase amount of complex carb and vegetable proteins in diet
131
smoking management
- enroll in a program to stop
- change daily routines associated w smoking to reduce desire to smoke
- substitute other activities for smoking
- ask family members to support efforts to stop smoking
132
physical inactivity management
- develop and maintain routine for physical activity that is performed at least 3-4 times a week
- increase activities to a level compatible w physical fitness. 30 min/daily.
133
stressful lifestyle management
- increase awareness of behaviours
- alter patterns that are conductive stress and rushing
- set realistic goals for self
- avoid excessive and prolonged stress
- take 20 min/day to mediate
- plan time for adequate rest and sleep
134
antiplatelet therapy: long term drug therapy
- long term aspirin therapy
- allergy to aspirin - clopidogrel (plavix)
- dual antiplatelet therapy:
1. ASA plus ticagrelor or plavix
2. pt recovering for ACS (usually for 1 yr)
3. pt who has undergone coronary artery stent placement
135
statins: long term drug therapy
- for all pt w an acute coronary syndrome - high intensity statin therapy is recommended
- atorvastatin 80 mg daily or rosuvastatin 20 or 40 mg
cholesterol total: <5 mmol/L
HDL (high-density lipoproteins): >1.55 mmol/L
LDL (low-density lipoproteins): <2.59 mmol/L
136
beta blockers long term drug therapy
- decrease contractility
- decrease HR
- decrease afterload
- lower O2 demand and increase supply
- metoprolol, atenolol
137
ACE inhibitors or ARB's
- management of BP
- prevent remodeling of the L ventricle
- pts w HF or less than normal L ventricular ejection fraction, diabetes, and kidney failure
- ramipril, captopril
138
nitrates
- promotes peripheral vasodilation - decrease preload and afterload
- enhanced collateral blood flow
- dilation of large coronary arteries - increased perfusion to ischemic zones
139
CCB's
- coronary and peripheral vasodilation
- reduce contractility
- used in combo w beta blockers
- diltiazem, verapamil, nifedipine
140
describe complications post MI
1. arrhythmias
- ventricular tachycardia/fibrillation
- afib
- bradycardia and heart blocks
2. congestive HF
3. cardiogenic shock
4. papillary muscle dysfunction
5. ventricular aneurysm
6. pericarditis
7. PE
