UBC RCE Compiled Notes II Flashcards
What is rate of MI in EST? Death?
5/10 000, 1/10 000
What is normal increase in SBP per MET?
10% increase per MET
Criteria for Hypotensive Response?
-Decrease in SBP below resting BP
-SBP goes down by 10 or more points after initial increase
What is Heart rate reserve?
Age predicted max HR - Resting HR
**How to write an exercise prescription: 50-70%
-THR = ((Max HR - Resting HR) x 0.5) + RHR = Lower end
What is calculation for Chronotropic Index?
(Max HR - Baseline) / (Age predicted - Baseline)
< 80%
Definition of abnormal HR recovery?
Not going down 12 point in first minute of recovery
What is more predictive of CAD: CP or ST changes on EST?
CP
What are the absolute CI’s to EST? (9)
-Symptomatic Severe AS
-ACS in last 48h
-High risk unstable Angina
-Decompensated HF
-Myopericarditis
-PE
-Aortic Dissection
-Unable to walk
-Arrhyhtmia with HD compromise
Name all absolute indications to stop an EST?
-Moderate-Severe Chest Pain
-Pallor/Cyanosis
-CNS symptoms/Ataxia
-ST elevation in leads without Q waves
-Unstable Ventricular Arrhythmias
-Hypotensive response with signs of ischemia
-Patient request to stop
-Cannot safely monitor the patient
Describe the BRUCE protocol
Begins at a workload of 4 METS and increases the workload every 3 minutes by 3 MET increments
What is the prognostic significance of LBBB developing during Exercise? How about RBBB?
-LBBB: Predicts higher risk of death and major cardiac events
-RBBB: Associated with CAD, especially LAD disease
What happens to the following with EST?
-P wave
-PR segment
-QRS
-Q wave
-T wave
-U wave
-QT interval
-P wave: Magnitude increases
-PR segment: Shortens
-QRS: Increases in amplitude
-Q waves: Increase
-T wave: Decreases in amplitude
-U wave: No changes with exercise
-QT interval: Absolute QT decreases
What is equivocal STD?
> 1mm upsloping STD
Is it normal to have normalization of Early Repol with exercise?
Yes
Why is having Complete Heart Block a contraindication to EST?
Risk of precipitating VT
What is the most important prognostic variable on EST?
Exercise Duration: 1 MET greater exercise capacity is associated with a 12% reduction in risk of death
4 CI’s to using Persantine/Adenosine? Updated as per CP guidelines
-SBP < 90mmhg
-SBP > 200mmhg
-Mod-severe asthma with active wheezing
-Brady < 45bpm without a pacemaker
-2nd or 3rd degree AV block without a pacemaker
-Dypirimadole recent use
-Methylxanthine use in last 12 hours
-ACS in last 48 hours
When assessing Viability, what has the highest sensitivity for predicting Viability?
Improvement with Low dose Dobutamine
When assessing Viability, what has the highest specificity for predicting Viability?
Biphasic response (Wall motion better at low dose, worse at high dose)
What is viability determined by on DSE?
Improvement of at least one grade in 2 or more segments
5 high risk criteria on DSE?
2 on CCS statement, preferred for exam:
-2 or more inducible WMA’s
-WMA at low ischemic threshold (Dobutamine < 10mg/kg/min, or HR < 120 bpm)
Others in case they ask more:
-Peak LVEF < 45% AND Extensive ischemia
-Baseline LVEF < 35 % AND Extensive ischemia
-Transient Ischemic DIlatation
Describe the following Adenosine receptors (1, 2A, 2B, 3)
1- SA and AV nodal blockade
2A- Coronary Vasodilation
2B- Bronchoconstriction and Peripheral Vasodilation
3- Mast cell degranulation
What is unique about Regadenoson?
Selective 2A receptor agonist
6 High risk criteria on MPI?
-Large perfusion deficits (>10%)
-Increase lung or RV uptake
-Multiple Coronary territories
-TID
-LVEF < 45% at peak stress of LV decrease from baseline with ischemia
-Resting LVEF < 35% due to non coronary cause
What happens to Myocyte metabolism when there is low O2 supply?
Shift in metabolism from fatty acid metabolism to glycolysis (using glucose).
How is the change in metabolism in low flow states taken advantage of when assessing Viability with PET?
-Glucose transport and phosphorylation is easily tracked by the uptake and retention of 18-FDG, which can be detected by PET.
What is Hibernating Myocardium?
-Chronically dysfunctional, but has the ability to regain function through revascularization
What are 4 criteria that a hibernating myocyte needs to have?
-Adequate blood flow
-Intact cell membrane
-Intact mitochondrial membrane
-Preserved metabolic activity
What is the definition of Stunned myocardium?
Dysfunctional myocardium followed a brief ischemic insult that was followed by reperfusion
What % of myocardium is needed to have viability to have increase in LV function post revascularization?
for PET? 7%
What are the two results of PET and what do they mean with respect to viability?
-Mismatch = Absence of perfusion, preserved FDG -> viability
-Match = refers to absene of both perfusion and myocardial metabolism -> scar
Where is the pattern of scar on CMR with Fabry disease?
The LGE pattern is distinct with a basal-inferolateral wall predilection
What is CMR RV criteria for ARVC?
RVEDV > 110 ml/m2 in men and >100 ml/m2 in women
OR
RVEF < 40%
Describe the following in JVP?
a
x
c
x’
v
y
a = atrial contraction
x = atrial relaxation
c = bulge of TV/MV into RA/LA
x’= descent of the base of heart
v = passive filling of LA
y = rapid emptying of LA
What is Carabello’s sign?
> 10mmhg increase in arterial BP during pull back = critical AS
What happens to Aortic Stenosis Post PVC?
Large LV-aortic gradient, wider pulse pressure and persistently delayed upstroke of aortic pressure
What are three findings of severe AS on a hemodynamic tracing?
-Delayed arterial upstroke
-Late peak pressure
-Exaggerated anacrotic notch
What are 4 RA/JVP findings in CP?
-Prominent Y descent
-A and V waves equal in height
-Elevated
-+ Kussmaul’s sign
What is the classic finding in CP seen in the RV/LV filling?
-Square root sign/Dip and Plateau: Rapid early filling followed by abrupt cessation in early diastole (plateau)
What is the most specific hemodynamic criteria for Constriction?
Interventricular dependence leads to discordant LV/RV filling
What is different in the JVP waveforms in RCM compared to CP?
Prominent x and y descents in CP
5 hemodynamic differences between CP and RCM?
-Ventricular interdependence in CP not RCM
-Equalization of RV/LV end diastolic pressures in CP not RCM
-RVEDP/PASP > 1/3 in CP but not in RCM
-PASP elevated >55mmhg in RCM not in CP
-Rapid LV filling in CP (early filling wave > 7mmhg) in CP but not RCM
What is a large shunt by QP/QS?
> 2.0
Name three reasons for a ABI > 1.30
-Renal disease
-Long standing diabetes
-Heavily calcified arteries
What are 5 determinate of Plaque vulnerability?
-Location: Proximal and bifurcating lesions
-Inflammation in the atherosclerotic lesion
-Size of the necrotic lipid core
-Thickness of the fibrous cap
-Integrity of the fibrous cap
Describe the mechanism of Coronary Plaque Rupture?
Plaque rupture leads to intraplaque hemorrhage -> Exposure of highly thromboembolic material to circulating blood -> Platelet rich thrombus is formed at the site of rupture -> Following adhesion platelet activation ensues and release of procoagulant and vasoconstriction substances -> coronary artery constriction and platelet aggregation -> intrinsic and extrinsic -> coagulation cascade -> conversion of fibrinogen to fibrin
Name the three time courses for Stent Thrombosis?
Acute: 24 hours
Subacute: 1-30 days
Late: 30 days to 1 year
Very Late: > 1 year
What are three different UA presentations?
Rest angina
New onset angina of at least CCS III
Increasing Angina by 1 or more CCS class to at least CCS III
Name TIMI score (7)
Age > 65
Troponin elevation
ECG changes
3 CAD RFs
CAD established
Recurrent CP
ASA use in last 7 days
What is low, intermediate and high risk for TIMI and what risk does it correlate to ?
Low risk (0-1) : 5% 14 day MACE
Intermediate (2-4): 10-20% 14 day MACE
High: >4 : >20% 14 day MACE
Name 8 GRACE risk factors?
Age
Kilip class
SBP
HR
OHCA
ST changes
Troponin elevation
Creatinine
< 108 = 1% risk in hospital mortality
>140 = 3% risk in hospital mortality
Also estimated 6 month mortality
When should beta blockers be started in ACS?
< 24 hours (Class 1)
What is the pharmacology of Prasugrel?
-Prodrug, requires metabolism in a 1 step process, irreversible.
What are three contraindications to Prasugrel?
History of TIA/Stroke, Wt < 60kg, Age > 75
When does Prasugrel need to be discontinued before surgery?
7 days before OR
What is the pharmacology of Ticagrelor?
Reversibly binding P2Y12 inhibitor, binds to the allosteric site, and it is an active drug
What is dosing for UFH?
60 units/kg load and then 12 units/kg/hr infusion (ACT of 250-350)
If Fondaparinux is used for ACS treatment, what dose of UFH needs to be given prior to angiogram?
85 IU/kg
When should unstable patients get PCI? How about high risk but stable patients?
< 2 hours
< 24 hours
When should ECG be performed when STEMI is suspected?
Within 10 minutes
What should Clopidogrel dosing be for STEMI depending on if Lysed or Primary PCI?
-Lysis: 300mg then 75mg daily (No load if age > 75y)
-PCI: 600mg then 75mg daily
What is Prasugrel dosing?
60mg po daily and then 10mg daily
What are the indications for primary PCI in STEMI?
STEMI within 12h symptom onset (Class 1)
STEMI with failed Lysis (Class 1)
STEMI in CS regardless of timing (Class 1)
STEMI within 12-24h with ongoing symptoms/ECG evidence ischemia/HF (Class 2)
What is dosing of the following Lytics?
-Streptokinase
-TPA
-TNK
-Streptokinase: 1.5 million units over 30-60 minutes
-Alteplase/TPA: 15mg IV bolus then 0.75mg/kg IV infusion over 30 minutes
-TNK: weight based IV bolus x 1
What are the 9 CI’s for lytic?
Active bleeding
Bleeding diathesis
Uncontrolled Hypertension
Prior ICH
Stroke last 3 months
Spinal surgery last 2 months
Intracranial tumor
Aortic Dissection
Facial trauma
4 steps to reverse ACS anticoagulants in case of ICH?
-Cryoprecipitates
-Platelet transfusion for antiplatelets
-Protamine for UFH
-FFP
When should PCI be done after Lytic?
24 hours
What is the incidence of free wall rupture in the PCI era? Lytic Era? Account for total mortality?
-1%
-5%
-15%
What are the three types of Free wall rupture?
1) Occurs during the first 24 hours. Full thickness rupture.
2) Occurs 1-3 days post MI. Due to erosion of the myocardium at the site of infarction.
3) Occurs 5-7 days post MI. Aneurysm forms and ruptures at the border between infarcted and normal myocardium
Name 4 mechanisms of MR post MI?
-Pap muscle rupture
-LV dilation
-Ischemic papillary muscle dysfunction
-Severe RWMAs
When does pap muscle rupture occur post MI?
2-7 days
Which two populations should have NIV testing for CAD based on sex/age and chest pain characteristics?
-Adults > 30 with 2/3 features of classic chest pain
-Men > 40 or Woman > 60 with 1/3 symptoms
Name 4 high risk ECG criteria for EST?
-Sustained VT
-ST elevation
- 2 or more mm ST depression at low workload (5 METS) OR persisting into recovery
-Failure to increase to SBP > 120mmhg or sustained decreased > 10mmhg during exercise
Others:
-Unable to complete 5 METS
-Chest pain at low workload (<5 METS)
-More than 5 leads with ST Depression
-ST Elevation in Lead AVR
-Syncope on Treadmill
Name 6 MPI criteria
Increase pulmonary intake
TID
Multisegment Ischemia > 10% of the myocardium
Resting LV function < 35% not explained by ischemia
Resting perfusion abnormality > 10% of the myocardium
Severe stress induced LV dysfunction (Peak LV function < 45% or decrease in LVEF with stress.
Name 2 high risk Stress Echo criteria?
-Multiple segments of ischemia
-WMA abnormality developing at low dose of dobutamine (< 10mg/kg/min) or at a low heart rate (<120 bpm)
Others:
-Resting LVEF < 35% not explained by a non coronary cause
-Peak LVEF < 45% or decreased from baseline with extensive ischemia
-Transient ischemic dilation
-WMSI on effort > 1.7
Should echo be done in all patients with SIHD?
Yes (as per CCS 2014 guidelines)
Name 5 indications for revascularization in absence of symptoms as per ESC 2018 Revascularization guidelines?
-Left Main > 50%
-Proximal LAD > 50%
-Two or three vessel disease LVEF < 35%
-Large area of ischemia > 10%
-Singe remaining patent artery with stenosis > 50%
Name 4 indications for CABG > PCI
-3VD SYNTAX > 22
-LMCA SYNTAX > 32
-Proximal LAD disease
-Multivessel disease with Diabetes
What is the SYNTAX Score?
-Coronary Dominance
-Which artery is the lesion in
-CTO
-Trifurcation
-Bifurcation
-Severe Tortuosity
-Length > 20mm
-Heavy Calcification
-Thrombus
What is the definition of Heart failure?
A clinical syndrome with abnormal heart function resulting in, or increasing the risk of clinical symptoms and signs of reduced CO and pulmonary/systemic congestion at rest of with stress
Describe the AHA staging for heart failure?
A: At risk of structural heart disease (HTN, Cardiotoxic meds, DM, CAD etc)
B: Structural heart disease but without symptoms of HF
C: Structural heart disease with prior or current symptoms of HF
D: Refractory HF requiring specialized interventions
What does ischemia do to the contractile proteins/myocytes?
-Ischemia results in depletion of ATP and leads to failure of myosin (thick filament) to detach from actin (thin filament) -> this results in stiffening/diastolic dysfunction
Describe excitation-contraction coupling in the myocyte
-During the plateau phase of the action potential, extracellular calcium enters the myocyte and binds to ryanodine receptors, which leads to larger calcium release from the sarcoplasmic reticulum and initiates contraction
-In the setting of sympathetic stimulation ryanodine receptors can be phosphorylated which increases calcium flux and cardiac contractility
-Myocardial relaxation requires all calcium to be removed from the cytoplasm, which requires ATP
What changes the ESPVR and EDPVR?
Contractility (Slope increases with positive inotropes)
Not affected by pre load or after load
What leads to changes in the End Diastolic PV relationship?
Diastolic dysfunction/Impaired relaxation- Ischemia, fibrosis, hypertrophy, infiltrative disease
Leusotropy would improve it
What are the three determinants of MVO2?
Wall stress, Contractility and Heart Rate
What is LaPlace’s law?
Wall Stress = Intracavitary Pressure x (Radius/Wall Thickness)
So Wall thickness increases in an attempt to reduce wall stress
Name 5 Neurohormones involved in ventricular remodeling?
-Norepinephrine
-Angiotensin II
-Aldosterone
-Vasopressin
-Endothelin-1
Review Clinical factors increasing risk of TDP when Long QT seen on ECG
Review causes of Restrictive CMO
5 reasons to choose surgery over lytic for PV thrombus?
-Patient preference
-Access to surgical expertise
-CI to lytic
-Large clot > 0.8 cm
-Low surgical risk
-NYHA IV
-Recurrent Thrombosis
-Concomitant CAD in need of revascularization
