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ACEM Fellowship > Cardio > Flashcards

Cardio Flashcards

1
Q

What is the pathophysiology of AMI

A

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

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2
Q

What are some non traditional risk factors for ACS

A

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

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3
Q

What are some risk factors for an atypical presentation of ACS

A

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

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4
Q

HFA risk tool

A

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

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5
Q

Why are Risk Assessment tools for ACS recommended?

A

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%

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6
Q

What is the TIMI score

A

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

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7
Q

What is the ADAPT protocol

A

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

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8
Q

What is the HEART score

A

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

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9
Q

What is the GRACE score

A

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

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10
Q

What is the CRUSADE score

A

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

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11
Q

Compare the HEART, TIMI and GRACE scores

A

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

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12
Q

What is EDACS?

A

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

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13
Q

What are the 5 types of MI and how are they classified

A

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

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14
Q

What are some cardiac and non cardiac causes of elevated troponin

A

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

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15
Q

When should repeat troponins be taken

A

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

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16
Q

When can a single troponin be taken

A

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

17
Q

What are some high and low risk features of chest pain

A

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

18
Q

When should otpt follow up be organized for intermediate risk chest pain

A

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

19
Q

Who can not have an EST

A

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

20
Q

What are some other tests that can be used to diagnosed CAD

A

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

21
Q

What are the contraindications to fibrinolysis and who should receive it

A

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

22
Q

When should a pt have PCI post thrombolysis

A

Failed fibrinolytic perfusion <50% ST recovery at 60-90minutes, ongoing hemodynamic instability and ongoing ischemic chest pain should have immediate PCI

Otherwise within 24hrs

23
Q

What are the dosing for clexane, heparin and thrombolysis

A

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

24
Q

What is the diagnostic criteria of Takotsubo and what is the pathophysiology behind it

A

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

25
Q

What is secondary Takotsbuo

A

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).
26
Q

What are the causes of a pericardial effusion

A
27
Q
A

ACEM Fellowship (22 decks)

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