Cardiology Flashcards
What are the events of the ischemic cascade with increasing ischemic time (5)?
- Blood flow changes (can be seen on myocardial perfusion)
- Diastolic –> systolic dysfunction (wall motion abnormalities)
- ECG changes
- Symptoms
- Myocardial necrosis
What are the diagnostic tests for CAD?
- Functional
- stress: exercise or drugs (inotropes, vasodilators)
- test: ECG, ECG+echo, ECG+nuclear - Structural
- angio
- CT angio
What are the contraindications to treadmill stress testing?
- Recent MI (< 4 days)
- UA
- Severe symptomatic LV dysfunction
- Likfe threatening arrhythmia
- Acute pericarditis
- PE
- Severe (or symptomatic) aortic stenosis
- Uninterpretable ECG (STD > 1mm, digoxin, pre-excitation, paced, LBBB)
What constitutes a positive stress test? What are the high-risk features?
Achieved 85% maximal HR
>1mm horizontal or down-sloping STD over multiple leads
High risk features:
1. >/=2mm STD; STD with <5 METS or persisting > 3min into recovery
- Exercise induced:
- STE
- VT/VF
- SBP drop by > 10 mmHg - Inability to increase SBP to > 120 with exercise
> 3% annual risk of death/MI if untreated
What is involved in an MPI? What can cause false negative results? What are contraindications to testing?
First line if unable to complete ECG stress test
Concept: coronary perfusion mismatch
-vasodilator (dipyridamole) given –> diseased vessels already max dilated –> flow “steal” by healthy arteries –> perfusion mismatch
False negative:
- Drugs that interact with dipyridamole (caffeine, theophylline)
- “Balanced ischemia” (severe triple vessel or left main disease)
Contraindications:
- active asthma/COPD (DP can induce bronchospasm)
- reversal agent: aminophylline
When is a coronary artery calcium (CAC) score indicated?
Risk stratification of intermediate risk FRS (10 - 19%) who would otherwise not be statin-candidates
-High CAC (>100) –> statin recommended
Not currently covered by OHIP or recommended due to radiation risk
What are the indications and contraindications for coronary CT angiogram (CCTA, different from CAC)? What does one do with the results?
Low dose CT under BB +/- IV nitro: target HR < 60, breath hold
Indications:
- workup of ischemic symptoms in low-intermediate pre-test probability patients
- risk stratification in patients with stable CAD
Contraindications:
- ACS
- severe structural heart disease (AS or HCM)
- usual CT precautions (contrast allergy, renal failure, pregnancy)
If suggestive of CAD –> medical treatment (ASA + statin)
What is the management of chronic stable CAD?
- Symptomatic improvement:
- BB
- CCB
- nitrates - Mortality benefit
- ASA (+/- low-dose rivaroxaban per COMPASS trial)
- smoking cessation, exercise, diet
- optimize risk factors: - HTN: ACEi
- DLP: high-dose statin, target LDL-C < 2 and 50% drop
- DM: A1c < 7%
- OSA: CPAP (but doesn’t seem to change CV outcomes)
OMT = revascularization (COURAGE, ISCHEMIA trials)
Revascularization if refractory to meds OR high risk structural disease (left main)
In stable CAD, when
is CABG preferable to PCI? Why?
CABG:
- left main (>50%)
- multivessel + DM
- multivessel + LV dysfunction/CHF
CABG v PCI:
- Stroke data conflicting between NOBLE and EXCEL
- less repeat revasc with CABG
- no clear mortality difference
What are the four pillars of ACS management (acute and long-term)?
- Immediate medical management
- Reperfusion
- Risk factor optimization
- Driving
What are the three component of immediate medical management in ACS?
- Antiplatelets
- ASA + 2nd agent
- loading doses: ASA 160 (chewed), Ticagrelor 180, Clopidogrel 300-600
- Ticagrelor CI if prior ICH
- thrombolysis –> ASA + Plavix (no ticagrelor or prasugrel) - Anticoagulation
- UFH, LMWH or fonda - Anti-anginal
- BB within 24h if stable
What are the reperfusion time-targets for ACS? When is PCI superior to fibrinolysis?
- PCI capable centre: FMC to balloon < 90 min
- Non-PCI capable centre: FMC to balloon < 120 min
- fibrinolysis chosen: FMC to needle 30min
PCI > fibrinolysis if:
- Timely (see above)
- Late presentation (12-24h after symptom onset)
- Cardiogenic shock
If lysis given, “drip and ship” (send to PCI centre for PCI within 24h)
What are the indications and contraindications specific to each 2nd antiplatelet agent (ticagrelor, clopidogrel, prasugrel)
- Ticagrelor
- first line for ACS
- more potent than clopidogrel: greater efficacy but higher bleed risk
- CI if prior ICH, active bleeding, mod-sev hepatic impairment, or in combination with CYP34Ai (ketoconazole, clarithromycin, ritonavir)
- Consider avoiding in heart block or bradycardia - Clopidogrel
- elective PCI (only agent studied)
- fibrinolysis (only agent studied)
- AFIB on DOAC - Prasugrel
- CI in age > 75, prior stroke (ischemic or bleed)
When should NSTEMI be reperfused?
Intermediate/high risk: early invasive strategy
- angio +/- PCI within 48h
- reduced rehospitalization and ischemia but not mortality benefit
Low risk or unclear diagnosis: non-invasive stress test (usually with functional imaging) first
What are the three options for PCI, their benefits and drawbacks?
- Plain old balloon angioplasty (POBA)
- rarely done - Bare metal stent
- endothelialize quickly (shorter DAPT required)
- higher rates of re-stenosis - Drug eluding stent
- take longer to endothelialize (longer DAPT required)
- lower rates of restenosis
What are DAPT durations (no AFIB)?
- Post-MI: 12 months
- min durations per below if urgent procedure required - Elective PCI
- BMS: 6 - 12; min 1
- DES: 6 - 12; min 3
DAPT > 1 year if well tolerated and low risk for bleeding
- evidence up to 3 years
- ASA + ticagrelor (60 BID) or clopidogrel (75 daily)
List the clinical and angiographic factors that constitute high risk for thrombotic events
Clinical:
- prior STEMI/NSTEMI
- DM
- CKD
- prior stent thrombosis
- smoker
Angiographic:
- multiple (3+) stents or lesions stented or use of a biodegradable vascular scaffold
- long lesion (>60 mm stent length)
- Complex lesion (bifurcation with 2 stents, stenting of chronic occlusion)
- LM or pLAD stent
- Multivessel PCI
What is the peri-operative management of anti-platelets?
Elective non-cardiac surgery:
- BMS: delay at least 1 month post-PCI
- DES: delay at least 3 months post-PCI
Pre-op:
- Hold Plavix/Ticagrelor 5 -7d prior
- continue ASA “whenever possible”
Post-op:
-Restart DAPT as soon as safe
Name four categories of post-ACS complications
- CHF
- Arrhythmias
- tachy: atrial, ventricular
- bradycardia, heart block (especially in inferior MI) - Mechanical
- pap muscle rupture/MR
- wall rupture (VSD, free wall)
- RV infarct (esp. inferior) - Pericarditis
- Dressler Syndrome: fever + pericarditis. Rx high dose ASA + colchicine
What are the driving restrictions post-ACS?
STEMI: 1 month/3 months (private/commercial)
NSTEMI + WMA: same as STEMI
CABG: same as STEMI
UA/NSTEMI w PCI: 48h/7d
UA/NSTEMI w/o PCI: 7d/1 month
Elective PCI: same as UA/NSTEMI w PCI
List 7 categories of causes of dilated CM
- Ischemic
- INfectious (viral, HIV, Chagas)
- Peri-partum
- Stress-induced (Takotsubo)
- Tachyarrhythmia
- Toxic (drugs, chemo, EtOH)
- Idiopathic (genetic: 30 - 40%)
List three mechanisms that result in restrictive CM and give examples for each.
- Infiltration: amyloidosis, hemochromatosis, sarcoidosis
- Myocardial fibrosis: CTDs like scleroderma
- Endocardial fibrosis: radiation, tumour, eosinophils
What are the management principles for HoCM (5)?
- Family screening & genetic counseling for 1st degree relatives
- Avoidance of hypovolemia/decreased LV volume
- Beta-blockers for everyone
- Procedure for some (septal ablation or myomectomy)
- ICD if:
- sustained VT or prior cardiac arrest
- FmHx of sudden death, LV wall thickness > 30mm, unexplained syncope
What are the cardiac manifestations of amyloidosis? List seven extra-cardiac manifestations.
Cardiac:
- CHF (from restrictive CM)
- syncope (ventricular arrhythmias)
- afib/flutter
- conduction system disease
- low-flow, low-gradient AS
May also have:
- Neuropathy
- LE neuropathy
- Carpel tunnel syndrome
- Autonomic neuropathy (orthostatic hypotension, gastroparesis, sexual dysfunction, sweating abnormalities) - Renal insufficiency/nephrotic syndrome
What are the normal pressures of the cardiac chambers?
RA: 7
RV: 35/8 (S/D)
PA: 35/12/20 (S/D/Mean)
PCWP (est. LAP/LVEDP): 12
What are the pharmacologic therapies to improve LVEF and mortality in HFrEF (6)?
- ACEi/ARB
- BB (carvedilol, bisoprolol, metoprolol succinate)
- MRA (spironolactone, eplerenone)
- ARB/neprolysin inhibitor (Entresto)
- SGLT2i
- ISDN-hydralazine (in black patients or intolerant to ACEi/ARB)
Avoid CCB when EF < 40%
- amlodipine generally safe but can worsen edema
- avoid diltiazem/verapamil entirely
When are SGLT2i indicated?
- T2DM plus:
- CAD
- HFrEF
- proteinuric CKD
- age > 50 + RF for CAD - HFrEF without T2DM
Describe the algorithm for the long-term management of HFrEF.
Triple therapy (ACEi/ARB + BB + MRA)
if T2DM: SGLT2i
–>
NYHA II - IV:
- switch ACEi/ARB to Entresto
- SR, HR > 70 –> ivabradine
- consider SGLT2i even if no DM
–>
EF > 35 –> CCM
EF < 35
–>
NYHA I - III:
-ICD/CRT
NYHA IV:
- consider hydralazine/nitrates
- referral for advanced HF or palliative care
When can beta blockers be safely used in HF?
NYHA IV pts should be stabilized prior to initiation
If a chronic med, continue in acute heart failure unless hypotensive or bradycardic
What are the indications for ICD for PRIMARY prevention? What are the indications for secondary prevention?
PRIMARY
LVEF = 35%
- despite 3 months of OMT
- min 1 month post-MI and 3 months post-revascularization
- NYHA II-III
- NYHA I + CAD + EF < 30%
- NYHA IV should NOT get an ICD if not predicted to improve further or are not candidates for advanced therapies (transplant, mechanical circulatory support)
SECONDARY
- Cardiac arrest
- Sustained VT + significant structural heart disease
- Sustained VT > 48h post-MI or revascularization
- Syncope + structural heart disease where syncope presumed 2’ to VT/VF
Above only apply if NO REVERSIBLE cause is found
*Sustained VT = VT lasting > 30sec or hemodynamically significant
What are the indications for CRT?
Major indications: LVEF = 35% AND -NYHA II - IV despite 3+ mo OMT -sinus rhythm -LBBB w QRS >/= 130
Consider if QRS > 150 (and no LBBB), afib, elderly/frail, chronic RV pacing with reduced EF
Add ICD (CRT-D) if criteria for ICD also met; otherwise CRT-P
Can upgrade PPM to CRT if criteria met
What are the principles of management for HFpEF?
- Treat HTN (usually ACEi/ARB)
- Diuretics for congestive symptoms
- Consider MRA for elevated BNP
- Treat comorbidities
- DM: metformin, SGLT2i reasonable. Avoid saxagliptin and thiazolidinediones
As a general principle, what are the follow-up imaging recommendations for asymptomatic, severe valvular heart disease?
Reimage every 6 - 12 months
What are the recommendations for medical therapies in valvular heart disease?
AS:
- treat HTN and DLP (neither prevents progression though)
- ACEi/ARB may reduce mortality post-TAVI
- note: severe AS is both preload and afterload dependent (stiff LV –> decreases CPP gradient)
- maintain BP and preload (caution with vasodilators/diuretics/afterload reducers)
- maintain sinus rhythm (need atrial kick to fill stiff LV)
- target low HR (maximizes preload)
AR:
- Treat HTN (preferably ACEi/ARB or Entresto)
- avoid slowing HR (maximizes regurgitant jet)
MS:
- Warfarin if prior CVA or LA thrombus or afib
- aim for slower HR to maximize diastolic filling
TR/MR:
-no Class I recommendations
What are the criteria for severe AS?
- Valve area < 1 cm
- Mean gradient > 40 mmHg
- Max jet velocity > 4 m/s
Note: may not have 3 or 3 in low-flow, low-gradient AS
What are the Class I indications for valve replacement in AS? When is TAVI recommended?
- Severe AS + symptoms
- Severe AS + LVEF < 50%
- Mod-severe + undergoing CVSx
- Symptomatic low-flow, low-gradient AS + LFEV < 50% (or EF > 50% IF AS most likely cause of symptoms)
TAVI:
- intermediate/high surgical risk
- age > 80
- life expectancy < 10 yrs
Contraindicated if comorbidities preclude benefit
-recommend palliative care if life expectancy with reasonable QoL < 1 year)
Note: all TAVI valves are bioprosthetic and need IE prophylaxis
What are the Class I indications for valve replacement in AR?
- Severe + symptoms
- Severe + LVEF < 55% (if no other cause of LV dysfunction found)
- Mod-severe + undergoing CVSx
May require AVR + ascending aortic replacement if aortic diameter > 45mm (more applicable to bicuspid AV patients)
What are the criteria for severe MS?
Etiology: 99% rheumatic
Severe MS:
- MV area < 1.5cm (very severe < 1cm)
- pulmonary artery systolic pressure > 50 mmHg
- Diastolic pressure half time (PHT) > 150 ms
What are the indications for surgical intervention in MS?
Percutaneous mitral balloon commissurotomy (PMBC) if:
-severe + symptomatic + favorable anatomy + can be performed at a comprehensive valve centre
=contraindicated if LA thrombus or moderate-severe MR
MV Sx (commisurotomy +/- repair or replacement):
- severe MS + symptoms + acceptable surgical risk + contraindicated/failed PMBC
- severe MS + other CVSx
What are the indications for surgical repair of MR? TR?
Primary MR surgical indications:
1. Severe MR + symptoms
- Severe MR + LVEF < 60%, LVESD > 40
No Class I surgical indications for functional MR; focus on GDMT
Severe TR:
-if undergoing left-sided valve surgery anyways
Describe medical management of valves following surgical replacement.
Mechanical valves
- lifelong warfarin
- goal INR varies (2.5 for current gen AVR; 3.0 for MVR, old AVR [ball in cage], or AVR with risk factors [Afib, CVA, LV systolic dysfunction, hypercoagulable state)
- DOACs CONTRAINDICATED
- post-op: bridge as soon as bleeding risk acceptable
Bioprosthetic:
- lifelong ASA
- warfarin + ASA for 3 - 6 months post-implantation (TAVI: can consider Plavix + ASA instead of warfarin + ASA)
- Afib: onset within 3 months of procedure –> warfarin; Afib > 3 months post-op –> DOAC or warfarin based on CHADS2 score
What are the management principles of a thoracic aortic dissection?
- HR control
- target HR < 60-65
- labetalol IV first line - BP control
- target SBP < 120
- can use nitrate in addition if needed - Definitive management by type
- Type A: ascending –> urgent surgical intervention
- Type B –> descending aorta –> medical mgmt (HR/BP control)
How often should thoracic aortopathy/aortic aneurysm be re-imaged? What modalities are used? What is the long-term management?
Aortic dilatation/aneurysm: serial imaging q6 - 12months
- depends on rate of change
- q6months of genetic aortopathy
Age < 50: MRI first line
- CT, TEE, TTE also options
- try to use same modality throughout
Long term management:
- Target BP < 140/90 (130/80 if DM)
- Marfan’s: use BB or losartan (otherwise no particular anti-hypertensive indicated)
Avoid fluoroquinolones (risk of rupture)
Operative management per size criteria (separate flashcard)
What are the size criteria for operative management of ascending aortic aneurysm?
Ascending aorta (cm):
- Degenerative: 5.5
- Bucuspid AoV: 5.5
- Marfan: 5.0
- Familial aortopathy: 4.5
- Other genetic syndromes: 4.2
- Undergoing CVSx: 4.5
What are the recommended AAA screening criteria? What are the pillars of management?
Screen all men age 65-80 once with US
Mgmt:
- Smoking cessation (only medical therapy that reduces risk of rupture)
- avoid fluoroquinolones (increase risk of rupture)
- surgical repair
Risk of rupture > risk of surgical repair once size > 5.5cm
-consider if > 5cm if other clinical risk factors (family history CTD, rapid growth, etc.)
How is pericarditis defined?
2+ of the following:
- pleuritic chest pain
- friction rub
- ECG changes (diffuse STE +/- PR depression without reciprocity)
- new/worsening pericardial effusion
Trop can by + in myopericarditis
List 7 categories of causes of pericarditis and give an example of each.
VITAMIN
Vascular - post-MI (Dressler’s)
Infxn - viral (coxsackie, echovirus, adenovirus; not ILI), TB, fungal
Toxin - procainamide, hydralazine, INH
Autoimmune - RA, SLE
Metabolic - hypoTSH, uremia, dialysis
Iatrogenic - radiation, post-CVSx
Neoplastic - mesothelioma, metastases, leukemia/lymphoma
When should pericarditis be admitted to hospital?
Patient factors:
- Immunocompromised
- Anticoagulated
Presentation factors:
- Trauma
- Subacute onset
- Fever > 38C
- Hemodynamic instability
Imaging/investigations:
- Myopericarditis
- Severe effusion (>20mm) or tamponade
What is the treatment for first episode and recurrent pericarditis?
First episode:
-High dose NSAID x 2 weeks (as needed until pain/CRP resolves)
+ colchicine x 3 months
Recurrence:
-same as first episode but colchicine x 6 months
Post-MI:
- ASA instead of NSAIDs
- high dose: 650mg PO QID
Note: steroids settle inflammation quickly but increase recurrence risk. Avoid unless immune-mediated etiology or clearly on-responsive/contraindications to ASA/NSAIDs
-still given colchicine in addition
Differentiate tamponade from constrictive pericarditis and restrictive CM. What are the physical exam findings that help distinguish each?
Constriction: fibrous pericardium limits expansion of cardiac chambers
- rapid early ventricular filling that abruptly stops as the “stretch limit” of the pericardium is reached (rapid Y descent; square root sign on cardiac cath)
- usually present with CHF
- exam: Kussmaul’s sign; usually no pulsus paradoxus, pericardial knock
Tamponade: accumulation of fluid in the pericardial space increases pericardial pressure exerted on cardiac chambers, impairing filling
- SICK patient
- Exam: blunted Y descent, pulsus paradoxus, Beck’s triad (hypotension, JVD, muffled heart sounds)
- no Kussmaul
Both are PERICARDIAL problems characterized by VENTRICULAR INTERDEPENDENCE
-increased R heart filling –> reduced L heart filling
Restrictive CM is a MYOCARDIAL problem that may resemble constriction (prominent Y descent)
-Kussmaul +, no pulsus
What is included in the basic workup for new Afib per CCS 2020 guidelines?
ECG - document rhythm (durr) Echo CBC, lytes (Mg, Ca), Cr, Coags, TSH LFTs (before amiodarone Rx) A1c, FBG, lipids
Describe the non-pharmacologic components of afib modifiable risk factor management.
- EtOH and smoking cessation
- OSA screen and treatment
- Weight loss (> 10% to BMI < 27)
- Exercise (aerobic 30m x 3 - 5d + resistance 2-3d + flexibility 10m x 2d)
- Comorbidity management (DM target A1c < 7%; HTN mgmt per comorbidity profile)
What are the principles around pharmacologic therapy in afib?
- Treat modifiable risk factors first
- Achieve rate control with BB, CCB or digoxin
- Afib w pre-excitation (WPW) –> cardioversion or procainamide
- Rhythm control preferred if
- QoL impaired
- hemodynamically unstable (cardiovert)
- hx of cardiovascular disease
In what populations are VKAs indicated for stroke prevention?
Valvular afib:
- mechanical valves
- rheumatic MS
- mod-severe non-rheumatic MS
Describe the anticoagulant recommendations for patients with afib and CKD.
Calculate CrCl using Cockroft-Gault
Stage 3 (GFR > 30): per usual
Stage 4 (15 - 29):
- DOAC > VKA
- apixaban and rivaroxaban approved
Stage 5 (< 15): no anticoagulation or antiplatelets for afib
DOSE ADJUSTMENTS:
Apixaban: 2.5mg BID if 2/3:
- age > 80
- weight < 60kg
- Cr > 133
Rivaroxaban
-15mg daily if CrCl 30 - 49
Dabigatran:
110mg BID if age > 75 OR CrCl 30 - 49
Edoxaban: 30mg daily if any of -CrCl 30 - 50 -Weight < 60kg -use of potent p-GP inhibitors
Describe the anticoagulation recommendations in patients with afib + stable CAD/PVD, ACS, and elective PCI.
- Afib + stable CAD/PVD
- CHADS65 0 –> ASA or ASA + low-dose riva (per COMPASSS)
- CHADS65 > 0 –> OAC - AFib + elective PCI (low risk for thrombotic events) OR Afib + ACS (no stent)
- CHADS65 0 – DAPT x 6-12m
- CHADS65 > 0 –> Clopidogrel + OAC x 1 - 12 months, then OAC alone - Afib + high-risk elective PCI or ACS
-CHADS65 0 –> DAPT
-CHADS 65 > 0 –>
“triple therapy”: DAPT + OAC x 1 day - 1month
THEN
“dual therapy”: Clopidogrel + OAC up to 12 months
THEN
OAC alone
What are the DOAC dosing considerations in dual and triple therapy pathway regimens for Afib?
- Dual pathway:
- normal dose apixaban, dabigatran or edoxaban
- rivaroxaban 15mg daily (10mg if CrCl 30 - 49) - Triple therapy:
- rivaroxaban 2.5mg BID
- apixaban 5mg BID (2.5mg if dose-reduction criteria met)
- warfarin (target INR 2 - 2.5)
Once on OAC monotherapy standard CVA-prevention doses apply
In what populations should OAC (that would otherwise be indicated) not be offered?
CP-C liver disease or with associated significant coagulopathy
Secondary AF
- exception: underlying “abnormal substrate” and high risk for recurrence
- reasonable to treat until reversible factor resolved (e.g., until euthyroid in thyrotoxicosis)
Individualize treatment decisions in cancer (DOAC generally > VKA) and frail elderly
What is the duration of anticoagulation post-cardioversion? When do you need to “pretreat” with 3 weeks of anticoagulation?
AC for 4 weeks post-cardioversion, then based off CHADS65 score
Anticoagulate for 3 weeks prior if:
- valvular afib
- onset > 48h ago
- onset 12 -48h + CHADS > 1
- onset < 12h ago + recent CVA/TIA
NOTE: if meeting above criteria but UNSTABLE, just cardiovert and start anticoagulation ASAP
When is a rhythm control strategy preferred to rate control per CCS 2020 Afib guidelines? What is involved in a rhythm control strategy?
Paroxysmal afib
Permanent afib and:
- recent onset (< 1 year)
- highly symptomatic or QoL impairment
- multiple recurrences
- difficulty achieving rate control
- arrhythmia-induced cardiomyopathy
EAST-AFNET Trial (2020) also support rhythm control in patients with cardiovascular disease
“Rhythm control” = cardioversion followed by antiarrhythmic drug
What are the options for long term rhythm control AADs?
EF < 40% –> amio
EF > 40% –> amio or sotalol
CAD –> dronedarone, sotalol, amiodarone
No CHF or CAD –> dronedarone, flecainide, propafenone, sotalol
Everyone: ablation as last line
When is left atrial appendage occlusion used for stroke prevention in afib?
patients who cannot tolerate anticoagulation and high CHADS
What are the indications for PPM? What are the indications post-ACS? When is PPM contraindicated post-ACS?
- Sinus node dysfunction
- symptomatic bradycardia or tachy-brady - AV block
- 3rd degree or Mobitz II
- alternating BBB
- symptomatic slow afib
- symptomatic AVB
Post-ACS:
- persistent 3rd degree
- persistent advanced/infranodal 2nd degree or 2nd degree + alternating BBB
- transient advanced 2nd degree AVB or 3rd degree AVB w associated BBB
- symptomatic 2nd or 3rd degree AVB
Contraindicated if:
- transient AVB in absence of intraventricular conduction defects
- transient AVB in presence of isolated LAFB
- new BBB or fascicular block in absence of AVB
- persistent asymptomatic 1st degree AVB with BBB or fascicular block
Describe the management of sustained the ventricular arrhythmias
Unstable –> cardiovert (ACLS)
Stable:
- amiodarone 150mg IV then 900mg/24h infusion
- structural heart disease: procainamide
Recurrent VT/VF or shock:
-IV lidocaine or additional amio boluses
Electrical storm (3+ episodes in 24h):
- BB (preferably NSBB)
- IV amiodarone
- sedation/anesthesia
- EP consult
Post-MI + reduced EF + non-sustained VT –> beta blocker
Polymorphic VT (even non-sustained) has high risk of sudden cardiac death and NEEDS FURTHER WORK UP -acutely: Mg bolus for polymorphic VT
What features help distinguish VT from SVT with aberrancy?
- Regular rhythm
- Positive QRS in aVR
- Capture beats
- Fusion beats
- RSR’ in V1 with taller left rabbit ear
When is stress testing indicated in the workup of syncope? When should carotid US be used? When should tilt-table testing be used?
Syncope that occurs before, during, or after exercise
Carotid US if focal neuro deficits preset
Tilt table if diagnostic uncertainty
What duration of cardiac monitoring is required in the workup of syncope?
Based off symptom frequency:
Daily –> 24-48h Holter
Weekly –> 2 - 14day (extended holter, external loop, patch monitor, mobile cardiac telemetry)
Monthly –> up to 1 month (same devices as for weekly)
= 3 years –> insertable cardiac monitors
What are the driving restrictions around syncope (private/commercial)?
Vasovagal: none (if not provoked sitting, typical vasovagal)
Recurrent, unexplained: 3 months syncope free / 12 months syncope free
What is POTS? What is the recommended workup and management?
Postural orthostatic tachycardia syndrome
Orthostatic intolerance: increase in HR by 30 within 10m of standing with no drop in BP
Workup
- look for secondary causes (hypovolemia, thyroid, etc)
- rule out systemic disease (Ehlers Danlos, autoimmune neuropathy)
- CBC, lytes, Cr, TSH, am cortisol
- no cardiac testing of diagnosis clear
Mgmt:
- exercise training
- liberalize salt (Na 10g/d) and water (3-4L daily)
- compression stockings (waist high)
- midodrine, fludrocortisone
How is FHH defined and treated?
Definition:
- LDL-C > 5
- Tendon xanthomas
- First degree relative with LDL-c > 5
- Premature ASCVD in pt or first degree relative (age < 65 women; < 55 men)
- presence of mutation known to cause FH
Treatment:
- healthy lifestyle (diet, exercise, weight, smoking, stress)
- risk factor modification (HTN, DM, obesity)
- Reduce LDL-c by 50% and < 2
Statin –> + ezetimibe –> + PCSK9 inhibitors
Cascade screening of family members
What are the CCS recommendations for cardiac screening of competitive athletes?
History
+/- physical exam
No routine ECG (only order if suggestive Hx or PEx)
Sport restriction if high risk of SCD (AVRM, HOCM w TV, aortopathy, etc.)
What is the differential of a systolic murmur? How do you differentiate between these etiologies?
Blowing quality –> MR v TR
TR: blowing, holosystolic, respiratory variation, cV wave
Chronic MR: blowing, holosystolic, displaced apex. May have “click” of MVP
Acute MR: JVP elevation, no respiratory variation, no apical displacement, patient in CHF
VSD: holosystolic, radiates from LSB –> RSB
AoS: radiates to carotid, diminished carotid pulse, +/- apical-carotid delay. Increases with increased preload (leg raise, squat) and decreased with decreased preload (valsalva)
AoSc: no features of AoS or HCM
HCM: double carotid pulse, “triple ripple” apical beat, non-displaced apex, +/- MR murmur. Increases with decreased venous return (valsalva), decreases with increased preload (leg raise, squat)
What is the differential of a diastolic murmur? How do you differentiate between these etiologies?
Low pitched rumble: likely MS
- opening snap (apex, after S2)
- may be Austin-flint murmur (“functional MR”)
High pitched: likely AI
- best heard @ RUSB
- signs of pHTN or dilated LV to determine acuity
- Austin-Flint murmur @ apex
- widened pulse pressure
- murmur shortens as severity increases
What are the treatment principles of HOCM?
Optimize volume status
Beta blockers (lower HR –> more diastolic filling time)
+/- diisopyramide (reduces contractility)
Avoid afterload reducing agents (ACEi) and diuretics
What are the best physical exam findings to rule in and out aortic stenosis?
Rule in:
- slow rate of rise of carotid pulse (LR+ 2.8 - 130)
- mid-to-late peak murmur (LR+ 8 - 101)
- soft S2 (LR+ 3 - 50)
Rule out:
-absence of radiation to right carotid (LR 0.05 - 0.10)
What are the risk factors for sudden cardiac death in HOCM?
Family history of SCD Spontaneous sustained VT Cardiac arrest (VF) Unexplained syncope LV thickness > 30mm Abnormal exercise BP, NSVT (on Holter)
Differentiate the physical exam findings of ASD from VSD
ASD
- wide, fixed split S2
- may have diastolic or systolic murmur of increased flow over tricuspid or pulmonic valve
VSD:
- holosystolic
- 3-4th intercostal
- thrill
- small defect –> louder murmur
What are the best tests to rule in or out tamponade?
Rule in:
-pulses > 12 (LR+ 5.9)
Rule out:
- absence of pulses > 10-12 (LR- 0.03)
- tachycardia (Sn 77%)
- elevated JVP (Sn 76%)
Not helpful: hypotension (Sn 26%), diminished heart sounds (28%)
What is the differential diagnosis for positive pulses paradoxus?
- Cardiac tamponade
- Severe asthma
Also described in RV infarct, PE, severe pectus excavatum
Which comorbidities imparted the most risk of developing severe COVID-19? What is the mortality and morbidity of patients admitted with COVID-19 with positive cardiac injury markers?
- HTN (30%)
- T2DM (15%)
- CAD (10%)
Interestingly COPD 3%
50% mortality if trop +
-60% developed ARDS compared to 15% without trop +
Which are the most useful tests to rule in or out PAD?
Rule in:
- pulse deficit (LR+ 4.7)
- bruit (LR+ 5.6)
- cool to touch (LR+ 5.9)
- wounds/sores (LR+ 5.9)
- discoloration (LR+ 2.8)
Rule out:
-absence of pulse abnormality (LR- 0.38)
What is the management of PAD?
Non-pharm:
- Smoking cessation
- exercise
- self-foot examination
- wound care
Pharm:
- Antiplatelets (ASA or Plavix) if symptomatic (also reasonable if asymptoamtic)
- Statin
- ACEi; treat HTN
- DM treatment
- Cilostazol (PDE3 inhibitor): improves symptoms and walking distance
- contraindicated in CHF
- Only anticoagulate for acute limb ischemia: don’t anticoagulate solely for PAD to reduce cardiac events
- Consider rivaroxaban 2.5mg BID + ASA
Revascularization:
- critical limb ischemia (minimize tissue loss)
- life-style limiting claudication with inadequate response to OMT
