Cardio Flashcards
What is the pathophysiology of AMI
Inadequate perfusion to meet myocardial oxygen demand causing cell necrosis and death. (Myocardial oxygen demand determines by HR, afterload, contractility and wall tension)
More commonly caused by UNSTABLE fibro-fatty plaques (lipid rich core with fibromuscular cap) can spontaneously rupture and result in cascade of inflammatory event, thrombus formation and platelet aggregation causing acute obstruction.
Alternatively STABLE fibrous plaques that don’t cause symptoms until they are occluding the vessel
What are some non traditional risk factors for ACS
CKD ( in grace score)
Autoimmune (SLE, RA, etc)
Field radiation or chemo
Female specific - PET, GDM, Preterm delivery
HIV
Antipsychotics and hx of mental health
Indigenous
Compliance and ability to follow up for otpt investigations
What are some risk factors for an atypical presentation of ACS
Women
Non caucasian
DM
Elderly (especially >85 would present with faitgue, dysponea, confusion or syncope)
Dementia
Intellectual disability
Risk of delay in diagnosis with worse outcomes/prognosis and increased risk of complications
HFA risk tool
Combination of hx, exam and troponin and ECG changes
Findings to predict 30-day MACE for pts
High sensitivity >78% (NPV 98%) pts but low specificity (~10%) (PPV 23)
Advantage - easy tool for use in various different centers and accessible to inexperienced and junior doctors
Disadvantages - poorly defined intermediate risk group. Given poor specificity, large number of pts will be categoriesed to high risk
Why are Risk Assessment tools for ACS recommended?
Allows quantification of risk for 30-day major adverse cardiac event (MACE)
Reduce misdiagnosis and inappropriate discharge from 2-8% to less than 1%
Increase absolute rates of early discharge for low-risk pts by up to 20-40%
What is the TIMI score
Estimates mortality for pts with unstable angina and NSTEMIs
Used in ED to help risk stratisfy pts for potential otpt management with presumed ischemic chest pain within the next 1 -2 weeks
Originally derived from pts with known UA or NSTEMI
5% risk of adverse outcome within 14 days for score of 0, so HEART score better for risk stratifying low risk pts
THREAAT
T - Troponin
H - History of CAD >50% stenosis
R - Risk factors >2
E - ECG ST 0.5mm changes
A - Aspirin within 7 days
A - Age over 65
T - Two episodes of CP within 24hrs
What is the ADAPT protocol
Accelerated diagnostic protocol using TIMI score with 0 and 2hr ECGs and troponins to identify who can safely be discharged home for otpt followup
Low risk 0-0.3% risk MACE in 30days
Intermediate (normal trop, ecg and TIMI 1) 0.8%
High risk 15.3%
Included pts >18 with at least 5 minutes of chest pain
Has a sensitivity of 99.7% for identifying low risk pts
False negative of 3% if TIMI 1
Modified ADAPT (highly sensitive troponin) uses TIMI 0 or 1 for low risk
Recommended by National Heart Foundation Australia and Cardiac Society of Australia and New Zealand when sensitive or highly sensitive troponins available
What is the HEART score
Risk stratification with UNDIFFERENTIATED chest pain in pts >/= 21yrs for risk of MACE at 6 weeks
Outperforms TIMI and GRACE in identifying low-risk pts
Needs experience taking detailed chest pain history and interpreting ECGs
Less sensitive at detecting high risk pts compared to GRACE
Not to be used in new ST elevation or clinically unstable pts
Combined with 0 and 3hr troponins to develop HEART Pathway
What is the GRACE score
Predictor of mortality in pts with known ACS in hospital, at 6 months and for GRACE 2.0 at 3 yrs.
Complex and time consuming with variables difficult to calculate without using electronic device
Useful in risk stratifying mortality in pts with known ACS but not to determine whether a pt with chest pain can be discharged for opt managment
Uses:
Age
HR and BP
ECG and trop
Killip class
Cr and Cardiac arrest on admission
What is the CRUSADE score
Risk stratify pts with NSTEMI and STEMI for major bleeding prior to initiation of treatment
Defines major bleeding as intracranial, intraperitoneal, hematocrit drop >12% or need for RBC transfusion
Sex (female worse)
HR and SBP
Hemocrit and Cr Clearance (most points for CrCl<15)
Hx of DM and Vascular disease
CCF on presentation
Compare the HEART, TIMI and GRACE scores
Aiming of scoring systems is to reduce risk of harm from misdiagnosis and inappropriate discharged for pts with ACS to <1% from 2-8% as well as increase rates of early discharge with low-risk pts (up to 40% of ED chest pain presentations)
HEART score developed for UNDIFFERENTIATED chest pain risk of MACE at 6 weeks
Quick and easy to use
Good sensitive for low-risk pts NPV 96-99
Subjective score on hx component means less reliable in junior or untrained clinicians
TIMI derived from pt with known unstable angina/NSTEMI to determine risk of MACE in 2 weeks and whether a pt may be eligible for otpt management
Part of the ADAPT pathway recommended by the National Heart Foundation Australia
Lower specificity so can overestimate risk
GRACE score is used to determine mortality for pts with known ACS in hospital, at 6 months and with GRACE2.0 at 3yrs
Comprehensive with accuracy in ling term prognosis and still recommended by Heart Foundation for determining risk stratification with pts with confirmed ACS
Complexity and time consuming to calculate
Poor sensitivity with low risk pts
What is EDACS?
Clinical tool to identify WHO can have a 0 and 2hr ECG troponin to investigate for ACS (instead of 0 and 6hr).
EDACS-ADP combines EDACS score with trop and ECG to determine who can safely be discharged
Sensitivity 99-100% for correctly identifying low risk pt
Able to identify more low risk pts then
ADAPT ADP and modified HEART
Provided no guidance on what to do for not pts not classified as low risk
USE IN
Pts over 18 presenting with normal vital signs and NO ongoing chest pain
What are the 5 types of MI and how are they classified
Defined by pathological, clinal and prognostic factors
Type 1 - spontaneous MI (atherosclerotic plaque rupture, ulceration, erosion or dissection resulting in intraluminal thrombosis)
Type 2 - MI secondary to ischemic imbalance from condition other than CAD eg spasm, tachy/bradyarrhythmia, anemia, hypo or hypertension, hypoxia etc
Type 3 - Death from suspected MI before biomarkers available
Type 4 - MI related to PCI or stent thrombosis
Type 5 - MI related to CABG
What are some cardiac and non cardiac causes of elevated troponin
CARDIAC
- Heart failure
- Myocarditis
- Cardiac contusion
- Cardioversion
- Takotsubo
- Rhabdo
- Angioplasty
NONCARDIAC
- Renal failure
- PE and severe PHTN
- Severe critical illness such as sepsis or resp failure
- Burns >30% TBSA
- Stroke and SAH
- Extreme exertion
When should repeat troponins be taken
When using POC troponin 6-8hrs post
When using sensitive lab assay
- 2hrs if TIMI score 0
- 6hrs if TIMI>0
When using highly sensitive lab assay
- 2hrs if TIMI 0 or 1
- 3hrs if TIMI >1
When can a single troponin be taken
Presenting with pain and symptoms resolving >12hrs prior to testing
Pts with inital highly sensitive trop < limit of detection and symptom onset >3hrs prior to testing
What are some high and low risk features of chest pain
HIGH RISK
- Ongoing or recurrent chest pain despite treatment
- Elevated trop
- New ECG changes (>0.5mm ST depression, transient >0.5mm ST elevation or new TWI >2mm in 2 or more contiguous leads. Also Wellens Syndrome)
- Hemodynamic compromise (SBP<90, cool peripheries, Diaphoresis, new mitral regurge or Killlip Class >1)
- Sustained VT
- Syncope
- Known LVEF<40%
- Prior AMI, PCI or CABG within 6 months
LOW RISK
- Age<40
- Atypical symptoms
- Remain symptom free
- Non known CAD
- Normal trop
- Normal ECG
When should otpt follow up be organized for intermediate risk chest pain
Within 1-2 weeks as long as they do not have a hx of significant failure to attend medical reviews.
Low risk pts may not need follow up
Who can not have an EST
Known BBB
LVH
Known severe valvular disease
Digoxin or beta blockers
Pre excitation syndrome
PPM
Women <50
Anemia Hb<90
Inability to achieve maximum predicted HR
Pros simplicity, widespread access, low risk and low cost. NPV 97-99% for AMI and death
What are some other tests that can be used to diagnosed CAD
TTE - needs to be performed during active chest pain. If regional wall abnormality not see unlikely cardiac cause
Myocardial perfusion scan - needs to happen within 2hrs of chest pain and if negative unlikely cardiac cause. Can assess exercise capacity and has high sensitivity 85-90% but potential false negatives and radiation exposure
CTCA - very sensitive (99%) with high negative predictive value in low -intermediate risk pts. Can not assess functional effect of stenosis nor exercise capacity
Difficult to organize in ED
What are the contraindications to fibrinolysis and who should receive it
CONTRAINDICATIONS
Prior intracranial hemorrhage
Known cerebral vascular malformation
Known intracranial neoplasms
Ischemic stroke within 3 months
Intracranial or spinal surgery with 2 months
Active bleeding or diathesis
Severe uncontrolled hypertension (>180/110) unresponsive to therapy
Suspected aortic dissection
RELATIVE CONTRAINDICATIONS
Active peptic ulcer disease
Pregnancy
Dementia
Stroke>3 months ago
Oral anticoagulation (warfarin)
Advanced liver disease
Chronic severe poorly controlled HTN
Diagnosed STEMI and
Expected delay >90minutes to PCI
Severe contrast allergy or poor vascular access limiting or delaying PCI
Streptokinase assosciated with higher rates of hypertension and intracerebral haemorrhage and due to high prevalance of streptococcal antibodies should not be used in Indigenous population
When should a pt have PCI post thrombolysis
Failed fibrinolytic perfusion <50% ST recovery at 60-90minutes, ongoing hemodynamic instability and ongoing ischemic chest pain should have immediate PCI
Otherwise within 24hrs
What are the dosing for clexane, heparin and thrombolysis
WITHOUT THROMBOLYSIS
Clexane 1mg/kg BD (0.75mg/kg in elderly)
Heparin (60units/kg) 4000units bolus followed by 12units/kg/hr
THROMBOLYSIS
Aleteplase 10mg bolus, 50mg over 1hr then 40mg over 2hrs (total dose <1.5mg/kg)
Clexane 30mg IV followed by 1mg/kg q12hr IF <75YRS OLD
No loading and 0.75mg/kg BD if >75
What is the diagnostic criteria of Takotsubo and what is the pathophysiology behind it
Transient dyskinesis of LV apical and or mid segment
Regional wall motion abnormalities beyond single epicardial vascular distribution
Absence of coronary artery stenosis >50% of culprit legion
New ECG changes or moderate troponin rise
Absence of phaeochromocytoma and myocarditis
Caused by acute stress response inducing catecholamine surge, sympathetic induced microvascular spasm
LV apex has highest density of sympathetic fibres so most susceptible
1/3 of pts underlying degree of LVOT increasing LV workload and worsening apical dyskinesis. More severe disease and poorer prognosis if they do
90% are post-menopausal women
30% have no identifiable stressors
What is secondary Takotsbuo
Common in ICU (20% of pts) following physiological stressors such as
- Post-cardiac arrest.
- Neurologic disorders (e.g., subarachnoid hemorrhage, status epilepticus, stroke).
- Brain death (may limit candidacy for cardiac donation).
- Sepsis.
- Respiratory failure (especially asthma or COPD, with excess beta-2 agonists).
- Autonomic instability, catecholamine excess.
- Autonomic nervous system manipulation (e.g., carotid artery surgery, radical neck dissection).
- Poisoning (e.g., sympathomimetic overdose), withdrawal.
- Surgery.
- Trauma.
- Endocrine emergencies (e.g., pheochromocytoma, thyrotoxicosis, adrenal crisis).
What are the causes of a pericardial effusion
