64. ACS Flashcards
ACS - what does this refer to?
constellation of clinical diseases occuring as a result of myocardial ischemia or infarction:
unstable angina - AMI
What is the leading cause of death among adults in industrialized countries?
CAD
Of those who present and have an MI, how many die within 30d?
30%
What factors play into prognosis of mortality post MI?
extent of infarct
time to intervention
whether pt underwent revascularization
residual LV function
How many MI’s are missed in the ED?
2% of pt with ACS
What is stable angina?
not ACS - transient, episodic CP from ischemia typically reproducible with physical or psychological stress
Canadian Cardiovascular Society Stable angina: class I defn
no angina with ordinary PA
Canadian Cardiovascular Society Stable angina: class II defn
minimal limitation of normal activity as angina occurs with exertion or emotional stress
Canadian Cardiovascular Society Stable angina: class III defn
severe limit of orginary PA as angina occurs even with exertion under normal physical conditions
Canadian Cardiovascular Society Stable angina: class IV defn
cannot do physical activity without discomfort as anginal sx occur at rest or very minimal PA
What is unstable angina?
new onset, occurrin at rest or minimal exertion
worsened from previous stable pain
What is rest angina?
at rest, lasting longer than 20 mins and occurs within 1 week of presentation
Increasing or progressive angina defn
previously known becomes for freq, longer duration, incr of one class (CCS) within last 2 months of at least class III
What are the pathophysiologic events underpinning unstable angina?
plaque rupture with thrombus and vasospasm
What is variant/Prinzmetal angina?
coronary artery vasospasm at rest with minimal fixed coronary artery lesions
may be relievedd by exercise or NTG
ECG looks like stemi
Myocardial infarction key defn
trop values above 99% ULN and at least one:
sx of MI
ECG changes: new stsegment or t wave change, development ofpathologic q wave
imaging eidence of loss of viable myocardium or regional wall motion abnormality consistent with ischemia
Angio or autopsy evidence of cornary thrombus
Type I MI defn
spont MI = ischemic from primary coronary event like a plaque erosion, rupture, fissuring or dissection with accompanying thrombus and vasospasm
Type II MI defn
demand supply mismatch
Type III MI defn
sudden unexpected cardiac death - including cardiac arrest, often with new MI signs - STsegment elevion, new LBBB
Type IV MI defn
assoc with coronary instrumentation - PCI
Type V MI
coronary artery bypass grafting
elevation of trop above 99% indicates periprocedural myocardial necorsis
If this incr is >5x ULN and: new pathologic q wave or LBBB, angiiographic documented new graft or native coronary artery oclusion or imaging evidencen ew loss viable myocardium
How is myocardial oxygen consumption defined?
HR
afterload
contractility
wall tension
What is characteristic finding of CAD?
thickening and obstruction coronary vessel artrial lumen by atherosclerotic plaque
Which atherosclerotic plaques are more likely to rupture?
fibro-lipid plaque - lipid rich core separated from arterial lumen by fibromuscular cap
How does thrombus formation occur in ACS?
endothelial damage and AS plaque disruption
platelet rich thrombus then occludes vesel lumen
What are considered most critical factors in infarction?
acute events of plaque rupture
plt activation
thrombus formation
rather than severity of underlying disease
ACS importnat factor: Vasospasm: what occurs in infarction?
central and CNS input incr, causing vasomo hyperactivity and spasm
symp stim may incr epi and serotonin and incr plt aggregation and neutrophil mediated vasoconstriction
Myocardial ischemia/infarction: what issues occur at the cellular level?
ca, o2, cellular elements to damaged myocardium cause further reperfusion injury, prolonged ventricular dysfunction or reperfusion dysrhytmias
neutrphils are key in reperfusion injuries as they occlude cap lumens, decr blood flow, accel inflamm response nad produce chemoattractants, proteolytic enzyme, ROS
Which populations may not have your classic ACS signs and symptoms?
women
OA
diabetes
Angina true defn
tightening
If pain does radiate down arm in ACS, where is typical?
ulnar
Classic sx of angina - “anginal equivalents”
dyspnea, nausea, vomiting, diaphoresis, weakness, dizziness, excessive fatigue, or anxiety.
Name 10 ddx of chest pain
AMI
stable angina
pericarditis
pneumonia
ptx
pleurisy
boerhaave
pud
esophageal spasm
cholecystitis/biliary colic
herpes
unstable angina
prinzmetal angina
myocardial/pulmonary contusion
pe
phtn
ao dissection
gerd
gastritis/esophagitis
MW tear
pancreatitis
msk pain
MC anginal equivalent sx
dyspnea
Nontradiational acs pain factors
atypical feat of pain, presence of equivalent sx
Traditional RF for CAD
age, tobacco smoking, hypertension, diabetes mellitus, hyper- lipidemia, and family history of AMI at an early age (usually <50 years).
Additional risk factors to consider include markedly elevated body mass index, artificial or early menopause, and cocaine (or other sympathomimetic agent)
Less common RF for CAD but important to consider
antiphospholipid syndrome
HIV
RA
SLE
List 5 early complications of AMI
dysrhythmias - brady, AV block; tachy - VF, VT
LV free wall rupture
papillary m rupture with acute MR
iv septal rupture
stroke - embolic
When does LV free wall rupture occur?
1/3 of cases first 24h, others 3-5d
esp anterior wall stemi
What finding is suggestive of LV free wall rupture?
pericardial effusion
When does IV septum or pap muscle rupture tend to occur?
3-5d post large MI
Findings of new iv septum rupture?
holosystolic murmur
flash pulmonary edema
HD collapse
infarct vs Dressler pericarditis defn
AMI, can occur early or in a delayed fashion; the former is termed infarct-related pericarditis, and the latter is known as post-MI or Dressler syndrome - 1 week to several months
ECG findings consistent with stemi: females of any age
new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: elevation 1.5 mm or greater in females of any age
ECG findings consistent with stemi: male <40y
new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: elevation 2.5 mm or greater in males less than
ECG findings consistent with stemi: male >40y
new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: 2 mm or greater in males greater than 40 years of age
Earliest electro graphic finding in STEMI
Hyper QT wave
What is the I point?
Junction between the QRS complex and the ST segment
What is differentiation of the SC segment elevation and ECG in BER?
Concavity of the ST elevation, more prominent as the corresponding S wave or negative deflection of the QRS complex becomes deeper
What is ST segment depression generally represent?
Sub endocardial ischaemia
Differential diagnosis of ST segment depression
Am I
Repolarization abnormality of LVH
Bundle branch block
Ventricular paste rhythm
Digoxin effect
Hyperkalemia
Hypokalemia
PE
ICH
Myocarditis
Related ST segment depression
Post cardioversion
Tacky dysrhythmia.
Pneumothorax
When is it normal to have tea wave and version i.e. what leads?
V1.
Possible and V2 to be normal
Definition of Wellen syndrome
The scheme, tea wave inversion: deep, symmetrical, T-wave, inversions, i.e. type one or by phasic T wave changes type two and the anterior precordial leads suggestive of myocardial, ischaemia and typically manifest in a pain-free state
Where is the occlusion in Wellen syndrome?
LAD
Differential diagnosis of T-wave inversion
ECS
Ventricular hypertrophy
Bundle branch block
Myocarditis
Pericarditis
PE
Pneumothorax
Wolff-Parkinson-White
Cerebral vascular accident
Hypokalemia
G.I. disorder
Hyperventilation
Persistent juvenile pattern.
Normal variant
What time does it take for pathologic Q wave to develop?
8 to 12 hours
Septal info leads
V1 and V2
Anterior versus lateral wall leads
Anterior equals B1 – before, lateral equals one, AVL, V5, V6
Right ventricular wall AMI will see what lead ST segment elevation?
V4R
What lead would you expect to see elevated in a posterior wall AMI versus depression?
Elevation in V-8, V9 and depression in V1 to be three
What artery serves the anterior wall of the heart?
LAD
ST segment elevation and leaded AVR is concerning for what occlusion?
Left main coronary artery and elevation greater than 0.5 MV is approximately 83% specific for left main disease
What is a de Winter tea wave?
Prominent tea wave with joint depression, producing ST segment depression seen in precordial leads, coupled with ST segment elevation in AVR
What does a de Winter tea wave indicate in terms of vessel concerning?
Proximal LAD
Leads two, three and AVF indicate inferior wall apart. What artery supplies this?
RCA
If patients with inferior wall hearts are not supplied by the RCA, what is the other artery that supplies them?
Left circumflex
What findings on an ECG are sensitive for a right coronary artery inclusion
Elevation inferior leads that is greater in lead three ST segment then lead to along with ST segment depression in AVL, one or both
What do EKG findings of ST segment elevation and lead V1 and the presence of an ST segment elevation inferior leads suggest?
Inferior am I with concomitant right ventricular infarction
What percentage of inferior or inferior lateral infractions also have posterior infarcts?
15 to 20%
What are indications that you may have a posterior infarction?
Reciprocal ST segment change in the right precordial leads, 1 to 3, horizontal, ST segment, depression, upright, tea, wave, tall, wide, our wave and our wave amplitude to S wave amplitude ratio greater than one
Post your leads eight and nine
What percentage of inferior heart attacks have associated infarction of the right ventricle?
33%
What do you expect to see in an inferior heart attack along with a right ventricular infarction?
ST segment elevation in Leeds, two, three, ABF and ST selling elevation in V1
With ST segment and elevation in lead three greater than leads to and AVF when coexists
Name six characteristics of BER that you will see on an ECG
ET segment elevation.
Upward concavity of the initial portion of the ST segment.
Notching of the terminal portion of the QRS complex at the JP point
Symmetric concordant T wave of large amplitude
Diffuse ST segment elevation.
Relative temporal stability over the short term
What ECG changes will you see with a left ventricular aneurysm?
ST segment elevation of any morphology typically in Leeds B1 to V6 and leads one and AVL.
Q waves may be present.
Typically the amplitude of a wave to the QRS complex exceeds 0.36 in any single lead equals more likely whereas less than 0.36 in all leads, likely ventricular aneurism
Sgarbossa criteria
ST segment elevation at least 1 mm that is concordant with the QRS complex.
ST segment depression at least 1 mm in lead V1, V2 or V3
ST segment elevation of at least 5 mm that is discordant with the QRS complex or in the modified version, excessive discordance by ST to S ratio of greater than 0.25 is considered diagnostic of AMI
What is Takutsubo?
Left apical ballooning ballooning syndrome with STE without obstructive CAD evidence
What type of MI, despite no STE needs urgent Revasc?
Acute posterior mi
Where do posterior leads go?
V8 and 9 at same level of v4 to 6 but under Scapula
What leads are used for RV MI? Which are most sensitive?
V1R to 6
V4R -
When should additional ecg leads be used?
St segment changed in more than one less
Equivocal changed in inferior or lateral leads
All inferior stemi
Hypotension in ACS
What is the recommended timing for a serial ecg?
Q20 mins
What is the definition of an elevated troponin?
Above 99% in healthy population
High trop but no ACS - list 5 other cardiology causes
HF
LVH
Myocarditis
Pericarditis
Non penetrating cardiac trauma
What non cardiac causes can raise troponin?
Physical exertion
Renal insufficiency
Multiple trauma
PE
Sepsis
Multi organ failure
What does bnp help with in ACS?
Long and short term mortality predictor
When should one exercise stress test someone?
Resolution sx
Low to mod suspicion ACS
False positive ddx of stress test
Aortic stenosis or insufficiency
HCM
Htn
Av fistula
Anemia
Hemoglobinopathies
Low CO states
Copd
Dig toxicity
Hyperventilation
MVP
bbb
Findings on pocus consistent with MI
Regional systolic wall abnormalities
Complications - ac MR, pericardial effusion, ventricular septal and free wall rupture, intracardiac thrombus
What medication is ordered for a stress test and what does it do?
Dipyridamole and adenosine to induce myocardial perfusion and reveal ischemia in susceptible patients
Myocardial scintegrsphy - what is this?
Tec-99 used to show slow redistribution to ischemic myocardium. High sn
What does the heart score tell you?
Risk of MACE within 30d
HEART score components ;list them
Score 0-2
History
ECG
Age
Rf
Trop
HEART score - history 0-2 points
0 - not sounding ACS
- 1 mixed omelet traditional and not
2 traditional
HEART SCORE - ecg
0 N
1 - no st Depn but has repop abnormal- bbb, lvh, dig effect, implanted RV pm, past mi +- unchanged repol abnormalities
2 - ste or depn typically new
HEART SCORE - age
0 - less than 45
1- 45-64
2- 65
HEART SCORE - RF
0 - none
1- 1-2
2- 3 or more RF or documented cardiac or systemic AS vascular disease
Ie DM, smoker, htn, high cholesterol, obesity, family hx of CAD
Systemic disease: pad, mi, pci, stroke
HEART SCORE - trop
0 - < discrimination level
1- elevated 1-3x normal
Trip > 3x normal
Heart score - at what level to consider adm vs not even if repeat trop negative?
<4 okay
>|= 4
5 key aspects of ACS physiology that guide management
- Endothelial damage through plaque disruption and irregular luminal lesions with shear injury
- Platelet aggregation
- Thrombus formation causing partial or total lumen occlusion
- Ca vasospasm
- Reperfusion injury caused by oxygen free radicals, ca and neutrophils
Time to benefit of STEMI and reperfusion therapy - how does this. Change over time?
Max within 1 hour
Less within 2 (40-60% of max benefit)
Then dwindled to 15-40% up to 6 hours
Under pci within ? Mins
90
If no access pci for stemi, receive fibrinolytic therapy within ? Mins of arrival
30
4 D’s to address delays in mi to cath
Door
Data ecg
Decision
Drug
Meds in ED for ACS
Aspirin first off
Once confirmed ACS then clopidogrel or ticagrelor
Antithrombin agent - heparin, enoxaparin
Stemi: fibrinolytic - streptokinase/tpa/tenecteplase
CP, opioids: NTG
What 4 meds may be considered for ACS once in patient?
Statin
Ccb
Beta blocker
Acei
What o2 level to target in ACS?
> /94%
What MI should you not give ntg in ?
Any if hypotension
But particularly inferior with Rv infarct as well
What SBP hold ntg at for mi?
<90
If ntg spray or patch not feasible, what level of infusion?
10 microgram per min titrated to pain sx
Can you give metoprolol in hf?
No
Aspirin mechanism ACS
Irreversible bind of cyclooxygenase and removed plt for 8-10d thus stopping production of thromboxane 2 which increases plt aggregation
Aspirin mechanism ACS
Irreversible bind of cyclooxygenase and removed plt for 8-10d thus stopping production of thromboxane 2 which increases plt aggregation
What type of meds are clopidogrel and ticagrelor
P2y12 receptor inhibit agent to stronger irreversible inhibit platelet aggregation for duration of plt life
ticagrelor does not require heparin activation
Concerns of ticagrelor over plavix
More bleed risk
How long should clopidogrel or ticagrelor be held if going for cabg?
24h min
Indication for glycoprotein iib/iiia receptor inhibitor ; abciximab in ACS?
Only useful if known undergoing pci
Not usually given ed
How does UFH work?
Antithrombin iii binding to inactivate ii/thrombin and activate factor X so cannot fibrinogen to fibrin
Also inactivate xai and is through antithrombin and interaction with plt
UFH dose
Initial bolus 60u per kg to max 4000 u and infusion 12u/kg/hr to goal aPTT 1.5-2.5
LMWH mechanism
Similar to UFH approx 1/3 mw of heparin - 1/3 bind to Antithrombin iii, remaining to factor xa
Why use LMWH over UFH
Easier admin
Greater bioavailability
More consistent therapeutic response in pt
Longer serum half life
Some greater benefit overall for high risk non stemi who are treated immediate without pci - vs if stemi and immediate recommend UFH
CI to heparin therapy in ACS
Ongoing hemorrhage
Predisposition to same
Fondaparinux: what is this?
Selective factor xa I
Fondaparinux pros and cons ACS
Pro: reduced risk hemorrhage, mi and death compared to heparins
Con; increased risk of cath associated thrombi during pci - needs UFH when invasive strategy chosen
When to give fibrinolytic?
Stemi NOT for NSTEMI
NOT for older than 75 as risk hemorrhagic stroke
Onset of ischemia within 12 hours (best within 6 hours)
Anticipated primary pci will not occur in timely fashion
NOT if bp persistently higher than 200/120
Relative CI if active diabetic hemorrhagic retinopathy
Not if cpr > 10 mins or extensive chest trauma
Hx of stroke or tia
Recent surgery (relative) - within 2-4 weeks
Watch closely if cardiogenic shock or hf (pci preferred5
What outcomes is pci better than fibrinolytic in?
More eligibility
Lower risk Ic bleed
Higher initial reperfusion
Earlier definition of coronary anatomy
Safe early hospital discharge
Is rescue pci significantly better than conservative management?
Not apparently per lit
If you can get pci within 90 min should you get fibrinolytic?
No!!!
Worse outcomes
Why is fibrinolytic therapy not an option in cardiogenic shock ACS?
Poor perfusion didn’t allow thrombus to be exposed
Most frequent cause of VT of Vfib OHCA
ACS
Unfavorable OHCA presentations
Unwitnessed arrest
Initial nonshockable rythm
No bystander intervention
Prolonged arrest time > 30 min
Ongoing CPR at Ed arrival
Abnormal studies: ph <7.20, lactate > 7
Age > 85
ESRD
Noncardiogenic cause of arrest.
