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Cardiology Flashcards

1
Q

Give an approach to picking a non-invasive test for CAD

A
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2
Q

List the absolute contraindications to EST

A

Mnemonic: I DO NOT STRESS

  • Inflammation (acute myocarditis, pericarditis)
  • Dissection (acute aortic dissection)
  • Ongoing unstable angina
  • No consent
  • Ongoing MI (within 2 days)
  • Thrombosis (acute PE, pulmonary infarction, DVT)
  • Severe AS (symptomatic)
  • Technical issues (ECG changes, etc..)
  • Rhythm (uncontrolled, hemodynamically significant arrythmia)
  • Endocarditis (active)
  • Systolic dysfunction (decompensated CHF)
  • Slow (physical limitations)
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3
Q

What is required to achieve a maximal stress test

A

Should reach 85% of age-predicted maximal HR*

*max HR=220-age

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4
Q

What constitutes a positive EST?

A
  • ≥1mm STE
  • ≥1mm STD (horizontal or downsloping)
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5
Q

List high-risk features on EST?

A
  1. Duke threadmill score -11 or less
  2. <5 METs achieved
  3. Low threshold angina/ischemia
  4. STE
  5. Severe STD ≥ 2mm
  6. Ischemia on ≥5 leads
  7. Ischemia ≥3min into recovery
  8. Abnormal BP response
    1. Failure to achieve SBP>120
    2. Drop in BP >10
  9. Ventricular arrhythmia
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6
Q

List 2 things that can cause a false-negative result on Persantine myooview

A
  1. Drug interactions with dipyridamole
    1. Caffeine
    2. theophylline
  2. Severe flow limiting triple vessel or LM disease (balanced ischemia)
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7
Q

What are contraindications to a Persantine myoview

A
  1. Active or severe asthma or COPD
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8
Q

What is the reversal agent for dipyridamole

A

Aminophylline

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9
Q

What is the coronary artery calcium score and what is it used for

A

It is used to further risk stratify patients with intermediate risk FRS patients >40 who are not otherwise candidates for statins. Can also be considered for low-risk FRS if FMHx of premature CVD and genetic DLP

CAC>100 = start statin regardless of FRS

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10
Q

List contraindications to CTCA

A
  1. ACS
  2. Severe structural heart disease (AS or HOCM)
  3. Usual CT precautions
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11
Q

How should chronic stable CAD be managed?

A
  1. Treat symptoms with medical therapy first
    1. ASA + Statin
    2. Plavix monotherapy if ASA intolerant
  2. Consider revascularization if refractory symptoms, high risk structural disease (i.e LM disease), LV dysfunction, severe MR
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12
Q

What treatments offer a symptomatic benefit in chronic stable CAD?

A
  • Beta blockers
  • CCB
  • Nitrates
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13
Q

What therapies help patients with chronic stable CAD live longer

A
  1. Smoking cessation, exercise, diet
  2. ?cardiac rehab
  3. Risk factor optimisation
    1. HTN
    2. DLP
    3. DMT2
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14
Q

Which patients with stable chronic CAD should be put on an ACEI?

A
  1. HTN
  2. DM
  3. EF<40
  4. CKD
  5. Reasonable for ALL patients
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15
Q

Which patients with chronic stable CAD should be on a BB?

A

EF<40 regadless of Sx

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16
Q

When should CABG be considered in chronic stable CAD?

A
  1. L main disease
  2. MV disease with DM
  3. Multivessel disease with LV dysfunction/CHF
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17
Q

What is the advantage of CABG over PCI?

A

Less repeat revascularisation, no clear mortality benefit

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18
Q

What medications should be given immediately to all patients with ACS?

A
  1. Antiplatelets
    1. ASA + Second agent (Ticagrelor, Clopidogrel, Prasugrel)
  2. Anticoagulation
    1. UFh, LMWH, Fonda
  3. Antianginal
    1. BB
    2. PRN nitrates
    3. (sparingly) PRN opioids
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19
Q

What are the contraindications to using Ticagrelor initially in ACS

A
  1. Previous intracranial hemorrhage
  2. Thrombolysis
  3. Active pathological bleeding
  4. moderate to severe hepatic impairment
  5. Combination with CYP34A inhibitors (ketonazole, clarithromycin, ritonavir…)
  6. Only Clopidogrel has been studied in elective PCI
  7. If patient is concurrently on DOAC, use clopidogrel
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20
Q

What antiplatelet agents shouls be used after thrombolysis

A

ASA + Plavix

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21
Q

What are the indications to perform primary PCI instead of fibrinolysis in STEMI?

A
  1. Timely
    1. PCI cabable hospital: FMC to baloon time <90min
    2. non-PCI capable hospital: FMC to balloon time <120 min
  2. Later presentation (12-24hrs)
  3. Cardiogenic shock
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22
Q

How quickly should fibrinolysis be administered following FMC?

A

30 mins

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23
Q

How quickly should a patient recieve PCI following fibrinolysis for a STEMI

A

24hrs

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24
Q

What is the window to give TNK in the case of a STEMI?

A
  1. can be given up to 24hrs
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25
Q

What risk scores can be used to risk stratify patients with NSTE-ACS

A

GRACE, TIMI

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26
Q

How should patients with NSTE-ACS and a moderate to high TIMI risk be managed once they are on all the ACS meds

A

PCI within 48hrs

*Reduces risk of rehospitalization but no mortality benefit

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27
Q

How should patients with NSTE-ACS and a low TIMI risk be managed once they are on all the ACS meds

A
  1. Non-invasive testing is reasonable first to determine the benefit of invasive strategy
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28
Q

What is the advantage and disadvantage of a BMS?

A
  1. Endothelialize quickly: Lower risk of stent thrombosis after 4 weeks
  2. Higher risk of restenosis
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29
Q

What is the advantage and disadvantage of a DES?

A
  1. Lower risk of restenosis
    1. Can be used in smaller vessels and CABG grafts
  2. Take longer to endothelialize=higher risk of in stent thrombosis
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30
Q

For how long should DAPT be continued after ACS?

A

minium of 12 months for all DAPT

For urgent procedures, can consider less

Can consider for up to 3 years if the patient is not at high risk for bleeding and tolerated the first year well

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31
Q

If DAPT is considered beyond the first year after ACS, what agents should be used?

A
  1. Clopidogrel
  2. Ticagrelor (60mg BID)
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32
Q

For how long should patients be on DAPT after an elective PCI?

A
  1. Aim for 6-12 months
    1. If that is impossible due to bleeding or surgery, minimum times are
      1. BMS: DAPT x 1 month then ASA indefinitely
      2. DES: DAPT x 3 months then ASA indefinitely
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33
Q

List high risk clinical features for thrombotic events post DES

A
  1. DM
  2. CKD
  3. Previous stent thrombosis
  4. Current smoker
  5. Hx MI
  6. Troponin + ACS
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34
Q

List high risk angiographic features for in stent thrombosis following PCI

A
  1. Multiple stents ore use of a biodegradable vascular scaffold
    1. ≥3 stents implanted
    2. ≥ 3 lesions stentes
  2. Long lesion length (>60mm total stent length)
  3. Complex lesions
    1. Bifurcation treated with 2 stents
    2. Stenting of chronic occlusion
  4. LM or proximal LAD stenting
  5. Multivessel PCI
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35
Q

What factors are associated with an increased bleeding risk in patients on DAPT?

A
  1. Need for OAC in addition to antiplatelets
  2. Advanced age (>75)
  3. Frailty
  4. Anemia (hb<110)
  5. Chronic renal failure (CrCl<40)
  6. Low body weight (<60 kg)
  7. Hospitalization for bleeding in the past year
  8. Previous stroke or IC bleed
  9. Regular need for NSAIDS or prednisone
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36
Q

For how long should elective, non-cardiac surgery be delayed following PCI

A
  1. BMS: 1 month
  2. DES: 3 months
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37
Q

For how long should semi-urgent, non-cardiac surgery be delayed following PCI

A
  1. BMS: 1 month
  2. DES: 1 month

* Individualize, not all patients can wait 1 month

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38
Q

How should DAPT be managed perioperatively in patients who are on such medications following PCI?

A
  1. Hold clopidogrel and ticagrelor 5-7 days pre-op
  2. Hold prasugrel 7-10 days pre-op
  3. Continue ASA perioperatively “whenever possible”
  4. Restart DAPT post-op as soon as deemed safe by surgical team
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39
Q

List post-MI complications

A
  1. Heart failure
  2. Arrythmias
    1. Tachy: Atrial, ventricular
    2. Brady: heart block
  3. Mechanical complications
    1. Papillary muscle dysfunction and acute MR
    2. Ventricular septal rupture
    3. Free wall rupture
    4. RV infarct
  4. Pericarditis
    1. Post-MI Pericarditis
      1. Early (5d)
      2. Delayed (2-8 weeks) (Dressler syndrome)
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40
Q

Which type of MI predisposes to heart block and RV infarction

A

Inferior

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41
Q

How are post-MI pericarditis treated?

A
  1. High dose ASA + colchicine
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42
Q

List the medications that should be started/optimised on all patients after an MI before they leave the hospital

A
  1. High potency statin
  2. BB
  3. ACEI
  4. +/-MRA
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43
Q

What non-pharmacological interventions should be offered after a patient leaves the hospital following ACS?

A
  1. Identify +/- optimize DM
  2. Smoking cessation
  3. CV rehab
  4. Driving restrictions
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44
Q

What are the driving restrictions following a STEMI

A
  1. Private driving: 1 month post-D/C
  2. Commercial driving: 3 months post-D/C
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45
Q

What are the driving restrictions following an NSTEMI with wall motion abnormalities?

A
  • Private driving: 1 month post-D/C
  • Commercial driving: 3 months post-D/C
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46
Q

What are the driving restrictions following UA or an NSTEMI with no LV damage

A
  • Private driving: 48hrs with PCI, 7days without PCI
  • Commercial driving: 7 days with PCI, 30 days without PCI
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47
Q

What are the driving restrictions following CABG

A
  • Private driving: 1 month post-D/C
  • Commercial driving: 3 months post-D/C
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48
Q

What are the driving restrictions following an elective PCI

A
  1. Private driving: 48hrs
  2. Commercial driving: 7 days
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49
Q

How are non-ischemic cardiomyopathies classified and what are the possible etiologies for each group?

A
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50
Q

What is the most common HOCM phenotype?

A

Asymetric septal hypertrophy

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51
Q

List symptoms of HOCM

A
  1. Chest pain
  2. Dyspnea
  3. Syncope
  4. Arrythmia
  5. Stroke
  6. CHF
  7. SCD
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52
Q

Other than hypertrophy, what is most often seen on ECHO in HOCM

A
  1. Dynamic LV outflow tract obstruction
  2. Systolic anterior motion MV → excentric MR
  3. Papillary muscle abnormalities
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53
Q

Who should be screened for HOCM

A
  1. 1st degree relatives of a case
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54
Q

What Rx can be used to manage chest pain syndromes, LVOT obstruction and SAM in HOCM?

A
  1. BB
  2. Second line : CCB, Dipyridamole
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55
Q

What interventions can be offered to patients with HOCM?

A
  1. Septal myomectomy
  2. ETOH ablation

*Not in all patients

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56
Q

What should be avoided in HOCM with regards to a patient’s volume status?

A

Avoid hypovolemia, low preload states

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57
Q

Who should be on a DOAC in the presence of HOCM and AFIB

A

Everyone (CHADS65 does not apply)

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58
Q

Which patients with HOCM should be considered for an ICD?

A
  1. Sustained VA or prior cardiac arrest
  2. FMHx of SCD, LV wall thickness>30mm, unexplained syncope
  3. NSVT or abnormal BP response on treadmill with other RF
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59
Q

What will reduce the murmur in HOCM

A
  1. Bradycardia
  2. passive leg raise
  3. handgrip
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60
Q

What increases a HOCM murmur?

A
  1. Valsalva or standing up
  2. Reduced afterload (ACEi)
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61
Q

What medications should be avoided in HOCM

A
  1. Afterload reducing agents (ACEi)
  2. Preload reducing agents (nitrate, diuretics)
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62
Q

List cardiac manifestations of cardiac amyloidosis

A
  1. Presyncope/syncope
  2. Atrial arrythmias (AF, sometimes ventricular arrythmias)
  3. bradyarrythmias
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63
Q

List extracardiac manifestations of cardiac amyloidosis

A
  1. Autonomic dysfunction
  2. Orthostatic hypotension
  3. Gastroparesis
  4. Sexual dysfunction
  5. Sweating abnormalities
  6. Neuropathy
  7. Carpal tunnel
  8. Renal insufficiency, nephrotic syndrome
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64
Q

What evaluations should be performed in suspected cardiac amyloidosis?

A
  1. ECG
  2. Echo
  3. +/- CMRI
  4. SPEP UPEP serum FLC
  5. Tc-99m-PYP scan : ATTR
  6. Genetic testing (genetic ATTR)
  7. +/- cardiac biopsy
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65
Q

What are possible ECG findings in cardiac amyloidosis

A
  1. Low voltages
  2. Pseudoinfarct pattern
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66
Q

How is cardiac AL-amyloidosis treated

A
  1. +++ diuretics
  2. AVOID:
    1. BB
    2. CCB
    3. ACE/ARB
    4. dig
  3. OACs for afib regardless of CHADS65 score
  4. Consider ICD, Get EP involved
  5. Chemo +/- ASCT
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67
Q

How is cardiac ATTR-amyloidosis treated

A
  1. +++ diuretics
  2. AVOID:
    1. BB
    2. CCB
    3. ACE/ARB
    4. dig
  3. OACs for afib regardless of CHADS65 score
  4. Consider ICD, Get EP involved
  5. Tafamidis or inotersen or patisiran +/- liver transplant
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68
Q

What investigations should be sent in AF?

A
  1. CXR
  2. ECG
  3. CBC
  4. lytes
  5. Cr
  6. Glucose
  7. TSH
  8. Echo
  9. BNP
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69
Q

Give a classification for causes of CHF

A
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70
Q

When should you suspect Cardiogenic shock in CHF

A
  1. Clinical + biochemical manifestations of tissue hypoperfusion
  2. SHOCK trial definition:
    1. Clinical
      1. hypotension (a systolic blood pressure of<90 mm Hg for at least 30 minutes or the need for supportive measures to maintain a systolic blood pressure of >90 mm Hg)
      2. end-organ hypoperfusion (cool extremities or a urine output of <30 ml per hour, and a heart rate of >60 beats per minute).
    2. hemodynamic criteria
      1. cardiac index of no more than 2.2 liters per minute per square meter of body-surface area
      2. pulmonary-capillary wedge pressure of at least 15 mm Hg
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71
Q

How is cardiogenic shock managed?

A
  1. Stop beta blockers and other antihypertensives
  2. Vasopressors and ionotropes
  3. May need mechanical support
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72
Q

How is acute pulmonary edema managed in the context of CHF?

A
  1. Identify underlying etiology
  2. Aggressive diuresis
    1. If congested, lasix
  3. If hypertensive or MR
    1. Short acting vasodilators
  4. May need inotropes
  5. NIPPV
    1. May require invasive ventilation
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73
Q

How are atrial arrythmias managed in the context of CHF?

A
  1. Determine chicken or egg (difficult)
  2. If overloaded achieve euvolemia
  3. If on BB, continue unless they are in shock
  4. If they are not on beta blockers, do not start them if they are overloaded or in shock
  5. Use short acting medications
  6. Dig can be helpfull
  7. If unstable, use ACLS algorythm
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74
Q

Regurgitate the shock grid

A
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75
Q

What investigations should be sent to determine the etiology of chronic CHF

A
  1. Echo + BNP
    1. BNP if unclear diagnosis and prognosis
  2. Assess for CAD (often cath)
  3. CMRI if non-ischemic
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76
Q

How is chronic HFrEF managed?

A
  1. Risk factor modifications and lifestyle interventions
    1. Exercise
    2. Salt restriction (2-3g)
    3. +/- fluid restriction (<2L/day)
    4. Smoking cessation
    5. EtOH avoidance
  2. Treat comorbidities
  3. Multidisciplinary care model
  4. Early ACP discussions
  5. Pharmacotherapy
  6. Consider interventional therapy
    1. ICD, CRT
    2. Surgery, Percutaneous MR repair
    3. Revascularisation if ischemic
  7. Reassess annually once stabilised
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77
Q

What is the pharmacotherapy for HFrEF?

A
  1. Quadruple therapy
    1. BB
    2. ARNI
    3. MRA
    4. SGLT2
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78
Q

In what timeframe should patients be on optimal doses of HFrEF pharmacotherapy

A

3-6 months

*can titrate q2-4 weeks

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79
Q

When should beta-blockers not be started on chronic CHF patients

A

NYHA IV

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80
Q

How long after stopping an ace inhibitor can you start an ARNI?

A

36 hours

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81
Q

List indications for SGLT2is in cardiology

A
  1. T2DM + established ASCVD
  2. T2DM, Age > 50 and risk factors for ASCVD
  3. T2DM, age >30, microalbuminuria
  4. LVEF<40 +/- T2DM
  5. HFpEF not yet in guidelines but trial based
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82
Q

What should you council your patients on if you are starting them on an SGLT2i?

A
  1. Genital mycotic infections, UTIs
    1. Do not start if they have an active genital/urinary infection
  2. Temporary reduction in GFR up to 15%, generally resolves in 1-3 months
  3. Hypoglycemia: Usually not seen unless they are also on insulin or a secretagogue
  4. HOLD SGLT2 when sick
  5. Risk of euglycemic DKA
    1. DO not start in decompensated DM
  6. Very rarely causes hypotension
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83
Q

What beta blockers are prefered in HFrEF?

A
  1. Bisoprolol
  2. Carvedilol
  3. Metoprolol succinate
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84
Q

When should Ivabradine be used in HFrEF

A

If on max Beta blockade, still having symptoms, hospitalized in last 12 months for CHF and HR >70

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85
Q

Is a washout period required when swiching from ARB to ARNI?

A

No

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86
Q

Are ARNIs contraindicated in the case of a history of angioedema?

A

Yes

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87
Q

What are the indications for ICDs in primary prevention?

A
  1. LVEF <30 (or 31-35 weak recomendation)
    1. as per HF guidelines:
      1. if ICM NYHA II-IV: EF ≤35
      2. if ICM, NYHA I: EF≤30
      3. If NICM, NYHA II-IV: EF ≤ 35
  2. After:
    1. 3 months optimal medical therapy AND
    2. 3 months post revascularization AND
    3. 40 days post-MI

*Caution in NYHA IV not expected to improve

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88
Q

What are the indications for ICDs in secondary prevention?

A
  1. Presence of 1 of these conditions with no reversible cause
    1. Cardiac arrest VT-VF (strong recommendation)
    2. Sustained VT in the presence of significant structural heart disease (strong recommendation)
    3. Sustained VT > 48hrs post-revascularisation. (weak recommendation)
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89
Q

What is the 1/3 rule for CRT?

A
  1. In non-carefully selected patients
    1. 1/3 improve
    2. 1/3 stay the same
    3. 1/3 worsten
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90
Q

List the slam dunk, may respond, and marginal recommendations for CRT

A
  1. Slam dunk
    1. In SR
    2. NYHA II-IV
    3. On GDMT
    4. EF <35%
    5. Typical LBBB
    6. QRS ≥130
  2. May respond
    1. In SR
    2. NYHA II-IV
    3. On GDMT
    4. EF<35%
    5. Non-LBBB
    6. QRS ≥150
  3. Marginal candidate
    1. Permanent AF
    2. Patients who require chronic RV pacing and have symptomatic HFrEF
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91
Q

When should a patient get a CRT-D as opposed to a CRT-P?

A

If they independently meet the criteria for an ICD

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92
Q

When should you worry about HFrEF patients and working them up for advanced therapy?

A
  1. ≥1 of these crit. met while on GDMT
    1. LVEF <25%
    2. Poor CPET results (Peak exercise VO2 <14 ML/kg/min)
    3. Progressive end-organ dysfunction
    4. recurrent HF hospitalizations
    5. Need to reduce or stop HF therapies
    6. Diuretic refractorieness
    7. Need for ionotropic support
    8. Worsening RHF or group 2 PH
    9. 6MWT <300m
    10. Increased 1 year mortality predicted by HF risk scores
    11. Persistant hyponatremia
    12. Cardiac cachexia
    13. Inability to perform ADLs
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93
Q

How should HFpEF be treated

A
  1. Largely based on symptom management and risk factor modification
    1. BP control as per HTN Canada guidelines
    2. Loop diuretics for coongestion
    3. Consider candesartan and MRAs
    4. No recommendations for ARNI
  2. Non-guideline based therapy
    1. Sx HF, EF>40, elevated BNP and either echo findings of diastology or HF hospitalisation
      1. empagliflozin 10
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94
Q

How should DM be managed in CHF patients

A
  1. Metformin 1st line agent
  2. Use SGLT2
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95
Q

Which oral hypoglycemiants should be avoided in CHF?

A
  1. Saxagliptin (other DPP4s ok)
  2. Thiazolinediones
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96
Q

How Should IDA be managed in CHF

A
  • If ferritin < 100 or if <300 and TSat <20%, give IV iron
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97
Q

How is CKD managed in CHF?

A
  1. Continue GDMT for patients on chronic HD
  2. Best data for ACEI/ARB/BB
  3. MRAs safe
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98
Q

How is OSA managed in CHF patients

A
  1. CPAP as per other guidelines
  2. No vent recommendations in central sleep apnea
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99
Q

How is exercise, smoking/ETOH managed in CHF patients

A
  1. Regular exercise
  2. Stop smoking
  3. stop drinking
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100
Q

What is the medical therapy for AS?

A
  1. Treat HTN as per standard guidelines
  2. Treat lipids as per guidelines
  3. ACEi/ARBs post TAVI
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101
Q

What is the pharmacological therapy for AR?

A
  1. Treat HTN (preferably with ACE/ARB)
  2. If prohibitive surgical risk and LV systolic dysfunction or symptomatic: ACE/ARB or ARNI
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102
Q

What is the pharmacological therapy for MS?

A
  1. VKA if prior embolic event or LA thrombus or AF
  2. Control of tachycardia can help symptoms
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103
Q

What is the pharmacological management of MR and TR?

A
  1. Treat HF as per standard guidelines
  2. Vasodilator therapy not recommended in asymptomatic primary MR and normal LV function
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104
Q

What are the 3 etiologies of AS?

A
  1. Bicuspid (young)
  2. Rheumatic (developing countries)
  3. Calcific (old)
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105
Q

What are the symptoms of AS

A
  1. Angina
  2. Syncope
  3. HF
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106
Q

What are the criteria to define severe AS?

A
  1. Mean gradient > 40
  2. Max gradient > 4
  3. AVA<1
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107
Q

What is low flow-low gradient AS

A

If the ventricle is weak, (HFpEF or HFrEF), you cant mount a gradient/velocities in the severe range

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108
Q

When should you be suspicious of low-flow low-gradient AF?

A

AVA<1 and non-severe gradient Vmax

Check the EF and SV

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109
Q

How is low-flow, low gradient AS diagnosed?

A

Dobutamine stress echo

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110
Q

What are the class 1 indications for aortic valve replacement?

A
  1. Severe symptomatic AS
  2. Severe asymptomatic AS with LV dysfunction
    1. EF<50
  3. Severe asymptomatic AS undergoing other CV surgery
  4. Symptomatic low-flow, low-gradient AS with LV dysfunction (EF<50)
  5. Symptomatic low-flow, low-gradient AS with LVEF >50 if AS is the most likely cause of symptoms
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111
Q

List indications for TAVI

A
  1. For intermediate, high and prohibitive surgical risk candidates
  2. age>80 or younger patients with life expectancy <10 years
  3. Consider for age 65-80 vs SAVR
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112
Q

When is TAVI contraindicated

A

if comorbidities preclude benefit

Palliative care is recommended instead if life expectancy with reasonable QOL <1year

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113
Q

What are 4 etiologies of acute AR

A
  1. Dissection
  2. Endocarditis
  3. Trauma
  4. Prosthetic valve dysfunction
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114
Q

List some of the etiologies of chronic AR

A
  1. Primary aortic problems
    1. Dilation
      1. AI conditions
      2. Syphilis
      3. Marfan
      4. Bicuspid
      5. HTN
    2. Dissection
    3. Trauma
  2. Primary valve problem
    1. Degenerative (calcific)
    2. Bicuspid
    3. Rheumatic
    4. endocarditis
    5. VSD
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115
Q

What are class 1 indications for valve surgery in AR

A
  1. Severe symptomatic AR
  2. Severe asymptomatic AR with LVEF ≤55% if no other cause for LV dysfunction identified
  3. Severe asymptomatic AR undergoing other CV surgery

*Severe AR defined by echo parameters

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116
Q

What are the etiologies of Mitral stenosis?

A

Almost always rheumatic

Others are MAC, radiation, autoimmune

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117
Q

What are the indications for anticoagulation in Mitral stenosis?

A
  1. Rhematic MS and AS
  2. Rheumatic MS and prior embolic event
  3. Rheumatic MS and LA thrombus
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118
Q

How does mitral stenosis respond to AF and high HR hemodynamically

A
  1. High HR: Loss of diastolic filling time
  2. AS: Loss of atrial kick
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119
Q

What are the criteria for severe MS?

A
  1. MV area < 1.5 (<1 is very severe)
  2. PASP>50
  3. Diastolic pressure half time ≥150
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120
Q

What are the class 1 indications for PMBC in AS?

A
  1. Severe symptomatic AS + favorable valve anatomy + can be performed at a “comprehensive valve centre”
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121
Q

What are the contraindications to PMBC in MS?

A
  1. LA thrombus
  2. ≥ moderate MR
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122
Q

What are the class 1 indications for MV surgery in MS

A
  1. Severe symptomatic MS + acceptable surgical risk + contraindicated or failed PMBC
  2. Severe MS and other CV surgery
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123
Q

What are the etiologies of acute MR

A
  1. Ischemia → Papillary muscle rupture
  2. Endocarditis
  3. Trauma
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124
Q

What are the etiologies of chronic MR

A
  1. Primary (degenerative, the valve is the problem)
    1. Valve leaflet
      1. MVP (myxomatous, fibroelastic deficiency)
      2. Rheumatic
    2. Annulus
      1. Calcification
    3. Chordae
      1. Trauma
      2. infection
      3. idiopathic
    4. Papillary muscle
      1. trauma
  2. Secondary (functional)
    1. Dilated or ischemic CMP
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125
Q

What are the class 1 indications for surgery in primary MR

A
  1. Severe, symptomatic primary MR irrespective of LVEF
  2. Severe asymptomatic primary MR with LVEF <60, LVESD ≥40

*Severe MR is defined using specific echocardiographic parameters

**Here the goal is to prevent LV dysfunction

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126
Q

Who should be considered for valve procedure in secondary MR

A
  1. Maximally tolerated GDMT including revascularisation and CRT before considering valve repair
  2. As per CCS, in patients with symptomatic HF despite GDMT and severe MR, should be evaluated for percutaneous mitral valve repair
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127
Q

What are the etiologies of TR?

A
  1. Primary
    1. Lead related
    2. Trauma
    3. IE
    4. rheumatic
    5. Carcinoid
    6. CTD
  2. Secondary
    1. PH related
    2. RV related
    3. RA related
128
Q

What are the class 1 indications for Tricuspid valve repair

A

Severe TR in patients undergoing left-sided valve surgery

129
Q

What are the anticoagulation indications in mechanical heart valves

A
  1. Lifelong therapy with warfarin
    1. INR 2.5 (2-3) for newer generation AVR with no other RF
    2. INR 3 (2.5-3.5) for MVR or older generation AVR(ball in cage) or AVR with risk factors
  2. Bridge when INR subtherapeutic
130
Q

What are the antithrombotic therapy indications in Bioprosthetic valves?

A
  1. Lifelong ASA
  2. For surgical bioprosthetic valves: Consider VKA + ASA x 3-6 mo
  3. For TAVI: Consider DAPT with clopidogrel or VKA 3-6mo
  4. If new-onset AF within 3 months of implantation: VKA
131
Q

What is the classic symptom of thoracic aortic dissection

A

Tearing or ripping chest pain radiating to the back

132
Q

List mimics to thoracic aortic dissection

A
  1. ACS
  2. Valvular heart disease
    1. AR
  3. Pericardial effusion, tamponade
  4. Syncope
  5. Stroke
    1. Focal neuro symptoms
  6. Renal failure
  7. Limb ischemia
  8. spinal cord injury
133
Q

What are the risk factors for thoracic aortic dissection

A
  1. HTN
  2. Vasculitis
  3. Valvular heart disease
    1. Bicuspid aortic
  4. Drugs
  5. Collagen disorders
    1. Marfans
    2. Ehler-Danlos
134
Q

What are the findings with the highest +LR for thoracic aortic dissection

A
  1. Focal neuro deficit (LR+ 6.6 -33)
  2. Pulse deficit/ differential BP (LR+ 5.7)
  3. Enlarged aorta or mediastinum on CXR (LR+ 2)
135
Q

What is the best first line imaging for Thoracic aortic dissection and what are alternatives?

A

CT Scan

alternative: MR, TEE

136
Q

What is the medical management of thoracic aortic dissection?

A
  1. Control HR
    1. Target HR<60
    2. IV Labetalol is a goood first line
  2. Control BP (once HR is controlled)
    1. Target BP < 120 systolic
  3. Agents: BB→CCB→nitroprusside→ACEI
    1. Preferentially use IV meds (easy on easy off)
137
Q

Who gets considered for urgent surgical management in thoracic aortic dissection?

A
  1. Type A:
    1. Involves Ascending Aorta
    2. Refer for urgent surgical intervention
  2. Type B:
    1. Not involving ascending aorta
    2. Medical management
138
Q

What are the criteria to diagnose acute pericarditis?

A
  1. At least 2 of:
    1. Pleuretic chest pain
    2. Friction rub
    3. Diffuse ST elevation +/- PR depression without reciprocal ST segment depression
    4. Presence of new/worst pericardial effusion
139
Q

What additional clinical evidence can be used in the diagnosis of acute pericarditis?

A
  1. Elevated inflammatory markers
  2. Inflammation on CT/MR
140
Q

What does it mean if the troponin is elevated in pericarditis?

A
  1. Myocardial involvement (myo-pericarditis)
  2. Higher risk
141
Q

What are the etiologies of acute pericarditis?

A
  1. Vascular: Post MI
  2. Infectious: viral
    1. Coxackie
    2. echovirus
    3. adenovirus
    4. flu
    5. parvo
    6. TB fungal
  3. Toxin: drugs
    1. Procainamide
    2. hydralazine
    3. INH
    4. minoxidil
    5. dilantin
  4. Autoimmune: RA, SLE…
  5. Metabolic: Uremia, HD, hypoT4
  6. Iatrogenic: Radiation, Post-CV surg
  7. Neoplastic:
    1. Mesothelioma
    2. Metastatic lung, breast, melanoma
    3. Leukemia
    4. Lymphoma
142
Q

When should patients with pericarditis be admitted?

A
  1. Immunocompromised
  2. Trauma
  3. OAC
  4. Myopericarditis
  5. Fever>38
  6. Subacute onset
  7. Significant effusion (>20mm) or tamponade
  8. HD instability
  9. Lack of improvement after 7 days of Tx
143
Q

How should Acute pericarditis be treated (first episode)?

A
  1. High dose NSAIDS 1-2weeks (as needed until pain/CRP resolves)
  2. Colchicine x 3 months
144
Q

How should Acute pericarditis be treated (recurrence)?

A
  1. High dose NSAIDS x 2 weeks (as needed until pain/CRP resolves)
  2. Colchicine x 6 months
145
Q

How should Acute pericarditis be treated (Post-MI)?

A
  1. High dose ASA (650 PO QID) instead of NSAIDS
  2. Colchicine
146
Q

How should Acute pericarditis be treated in pregnancy?

A
  1. <20 weeks
    1. ASA (1st line), NSAIDS, Tylenol, Pred
  2. >20 weeks
    1. Tylenol, pred (NO ASA OR NSAIDS)
  3. Breastefeeding
    1. Avoid ASA
  4. no colchicine
147
Q

When should steroids be used in acute pericarditis

A
  1. Immune mediated etiology
  2. Clearly non-responsive to NSAIDS/ASA
  3. CI to NSAIDS/ASA
148
Q

How is prednisone dosed in acute pericarditis?

A
  1. 0.25-0.5mg/day
  2. Consider Taper
149
Q

What can be used in advanced pericarditis cases where NSAID/ASA/pred fail?

A
  1. IVIG
  2. Anakinra
  3. azathioprine
  4. pericardiectomy (last line of defense)
150
Q

How should patients be councilled regarding exercise in acute pericarditis

A

Exercise restriction

151
Q

Compare and contrast constrictive pericarditis, tamponade and restrictive CMP

Which tends to be more unstable, which tends to present with CHF

A

Unstable: Tamponade

CHF: constrictive pericarditis

152
Q

Who should be screened for atrial fibrillation?

A
  1. General population
    1. Pulse based screening, all >65
    2. If pulse is irregularity irregular f/u with ecg
  2. Cardiac implantable electric devices
    1. Interrogate all high atrial rate episodes for possible AF
  3. Non-Lacunar embolic stroke of unknown source
    1. “at least 24hrs of ambulatory monitoring”
  4. Longer monitoring if AF is still suspected but not proven
153
Q

What are possible etiologies for AF?

A
  1. PE, pulmonary diseases, post-op, pericarditis
  2. Ischemic heart disease, idiopathic, IV central line in the RA
  3. Rheumatic valvular disease
  4. Anemia, alcohol, advanced age, autonomic tone
  5. Thyroid disease
  6. Elevated BP, electrocution
  7. Sleep apnea, sepsis
154
Q

What basic workup should be sent for new AF?

A
  1. Document rhythm
  2. ECHO: LV size + fcn, LA size + fcn, valves, LA size…
  3. CBC, Lytes, Cr, Coags, TSH (All)
  4. LFTs before prescribing amiodarone
  5. A1C, FBG, Lipid profile (comprehensive cardiac risk assessment)
155
Q

List the classification of AF symptoms

156
Q

When should a rhythm control strategy be pursued in AF?

A
  1. QoL impaired
  2. HD unstable
157
Q

How should AF with pre-excitation be managed from a rate/rhythm control perspective?

A
  1. DC cardioversion
  2. Procainamide
158
Q

Which patients should get anticoagulation in AF?

159
Q

DOACS should be used for anticoagulation in AF in every situation except…

A
  • VKA in
    1. Valvular AF
      1. Mechanical heart valves
      2. Rheumatic MS
      3. moderate to severe non-rheumatic MS
    2. Also consider VKA in new onset AF < 3 months after valce replacement (surgical or percutaneous)
160
Q

How should AF anticoagulation be managed in CKD?

A
  1. Stage 1-3 (GFR>30)
    1. Anticoagulate as usual
  2. Stage 4 (GFR 15-30)
    1. Anticoagulate as ususal
    2. DOAC>VKA
    3. Apixaban and rivaroxaban are safe in stage 4 CKD
161
Q

What are the indications for half dose apixaban (2.5 mg BID) in atrial fibrillation?

A
  1. 2/3:
    1. ≥80 years
    2. ≤60kg
    3. Cr>133
162
Q

What are the indications for dose reduction of dabigatran in atrial fibrillation? (110 mg BID)

A

>75 years or GFR 30-49

163
Q

What are the indications for dose reduction of edoxaban in atrial fibrillation? (30 mg daily)

A
  1. 1 of:
    1. CrCL 30-50
    2. ≤60kg
    3. Concurrent use of potent P-Glycoprotein inhibitors
164
Q

What are the indications for dose reduction of rivaroxaban in atrial fibrillation? (15mg daily)

A

CrCL 30-49

165
Q

How should anticoagulation be managed in patients with atrial fibrillation who also require antiplatelet therapy for CAD?

A

Applies to patients with CHADS65≥1

If CHADS65=0 treat with SAPT/DAPT as per guidelines

166
Q

Which patients are high risk for bleeding and which are high risk for ischemic coronary events

167
Q

How can the bleeding risk be mitigated in patients who require OACS and Antiplatelets

A
  1. Avoid ticagrelor, prasugrel
  2. Consider PPI
  3. Avoid NSAIDs
  4. If on VKAs target INR 2-2.5
168
Q

How are the doses of OACS adjusted based on what antiplatelets are used?

A
  • Dual pathway regimen
    • Rivaroxaban 15mg (10mg if CrCL 30-50)
    • Edoxaban, apixaban, dabigatran at normal dose
    • Warfarin target INR 2-2.5
  • Tripple pathway regimen
    • Warfarin daily (INR 2-2.5)
    • Rivaroxaban 2.5mg PO BID
    • Apixaban 5mg PO BID (dose reduce based on standard criteria)
169
Q

How should anticoagulants be managed in liver disease

A

No OAC in child-pughC cirrhosis or liver disease associated with significant coagulopathy

170
Q

How should anticoagulants be managed in cancer

A

Individualize

DOAC>VKA

171
Q

How should anticoagulants be managed in frail elderly patients

A

OAC for most

Individualize if high risk of bleed

172
Q

How should anticoagulants be managed in secondary AF

A
  1. No OAC
    1. Exceptions
      1. High risk for recurrence
      2. most patients getting AF during thyrotoxicosis until normal euthyroid state is restored
173
Q

How should anticoagulants be managed in pregnancy?

A

NO DOACS

Can consider Warfarin in T2-3 in unique circumstances

LMWH

174
Q

In which pregnant women should anticoagulation be considered?

A

AF + structural heart disease

AF + CHADS ≥1

175
Q

How should anticoagulation be managed around cardioversion?

176
Q

How is rate/rhythm management of atrial fibrillation achieved (give the pathway in the guidelines)

177
Q

What antiarrythmics should be selected for long term rhythm control in atrial fibrillation

178
Q

What antiarrythmic agents can only be used in acute rate control in atrial fibrillation? Which ones can be used both in acute and chronic

A
  1. Only acute
    1. Ibutilide
    2. Procainamide
    3. Vernakalant
  2. Both
    1. Amiodarone
    2. Flecanide
179
Q

In what type of AF should Dronedarone be avoided

A

Permanent AF

180
Q

Which medication should be avoided in patients on dronaderone

181
Q

Which antiarrythmic is associated with a “pill in pocket” approach

182
Q

Before using flecanide in a “pill in pocket” approach, what other medication should be given and why?

A

BB or CCB

Prevents 1:1 conduction

183
Q

What medication should be given prior to ibutilide

A

MgSO4 1-4g

184
Q

List the CIs to Sotalol

A
  • QTc >440
  • CrCL<40
  • EF<40
  • Other torsades RF
185
Q

When is vernakalant effective

A
  1. Recent onset AF (<48hrs)
186
Q

After what time in acute onset is amiodarone no longer recommended?

A

After 8hrs

187
Q

What are the side effects of amiodarone?

A
  1. IV risks
    1. Hypotension
    2. Bradycardia
    3. phlebitis
  2. Long term
    1. Transaminitis
    2. Pneumonitis
    3. Thyroid toxicity
    4. Derm toxicity
188
Q

What monitoring should be done in patients on long term amiodarone?

A
  1. LFTs q6month
  2. Thyroid q6month
  3. CXR annually
189
Q

What are the side effects of Dronedarone?

A
  1. Hepatotoxicity
190
Q

What monitoring should be done on patients on chronic dronedarone?

A

LFTs q3mo x 1year then q6mo

191
Q

What are CI to dronedarone

A
  1. CHF (LVEF <40)
  2. AV conduction delay
  3. prolonged QTc
192
Q

What are the side effects of flecanide

A

1:1 AV conduction

First dose should be given in a monitored setting

193
Q

List CI to flecainide

A
  • Structural heart disease
  • Ischemic CAD
  • EF<40
  • Liver failure
  • CrCL<35
194
Q

What are the side effects of ibutilide

A

Torsades, NSVT

195
Q

What are CI to ibutilide

A
  1. ACS
  2. reduced EF
  3. long QT
196
Q

What are the side effects of Procainamide

A
  1. Hypotension
  2. PVCs
  3. VT during infusion
197
Q

What is a CI of procainamide

198
Q

What are the side effects of sotalol

A
  1. QT prolongation
  2. torsades
199
Q

What monitoring should be done for patients on sotalol

A

ECG after 48-72hrs on therapy for QT

200
Q

What are the side effects of vernakalant

A
  1. Hypotension
  2. Bradycardia after cardioversion
  3. Abnormal taste
  4. Paresthesias
  5. Nausea
201
Q

What are CIs to Vernakalant

A
  1. Hypotension
  2. CHF
  3. Bradycardia
  4. recent ACS
  5. Severe AS
202
Q

In which patients should ligation of the LAA be considered

A

Only those who cannot tolerate OACs (i.e cerebral amyloid angiopathy and high CHADS AF)

203
Q

How should AF be managed in the context of WPW?

A
  1. If unstable: Electric cardiversion
  2. If stable: IV procainamide, ibutilide or electric cardioversion

*Avoid AV node blocking agents

204
Q

List the class 1 indications for PPM

A
  1. Symptomatic bradycardia
  2. Prevention of sudden death in asymptomatic patients
    1. High grade conduction system disease
205
Q

What etiologies should be considered in young patients with bradycardia?

A
  1. OSA
  2. Lyme
  3. Sarcoid
  4. Electrolyte abnormalities
  5. Thyroid
  6. genetic/inherited
206
Q

How should bradycardia be investigated

A
  1. Cardiac imaging in almost everyone
  2. EST if exercise induced Sx
  3. Tilt, carotid sinus massage if reflex induced symptoms
  4. In most, no great indication for EP studies
207
Q

When should a PPM be considered in heart block

A
  1. 2nd degree mobitz 2
  2. 3rd degree
  3. high grade AVB
  4. Permanent AF and symptomatic bradycardia
  5. Symptomatic AVB (spontaneous OR from required drug therapy)

NO PPM FOR

  1. Asymptomatic 1st degree AVB
  2. Asymptomatic mobitz 1
  3. Asymptomatic 2:1 AVB at the level of the AVN
  4. Reversible, non-recurrent causes
  5. Vagally mediated bradycardia
208
Q

When should a PPM be considered in sinus node dysfunction?

A
  1. Need to be symptomatic
    1. Sinus bradycardia, sinus pauses
    2. Requirement for GDMT
    3. Tachy-Brady syndrome
    4. Chronotropic incompetence
209
Q

How long after an MI can a PPM be considered?

A

Should undergo a waiting period. Generally 5 days

210
Q

What temporizing measures can be considered for bradycardia during the 5 day waiting period after an MI?

A
  1. Atropine
  2. Temporary pacing
    1. Medically refractory
    2. HD significant related to SND or AVB
211
Q

What are the indications for PPM post-MI?

A
  1. Mobitz II
  2. High grade
  3. Alternating BBB
  4. 3rd degree
  5. Other special circumstances
    1. Cardioinhibiitory carotid sinus syndrome
    2. Asystolic syncope during tilt testing
    3. Post-cardiac surgery
    4. post-TAVI
212
Q

What are class III recomendations for PPM after MI

A
  1. Transient AVB that resolves
  2. New BBB orr isolated fascicular block
213
Q

How is polymorphic VT/VF treated?

A

If unstable, do ACLS, Defibrillation

  1. Normal QT
    1. Acute ischemia
      1. ACS Tx
      2. Amio or lidocaine
    2. No ischemia
      1. amiodarone
  2. Prolonged QT
    1. IV Mg
    2. Overdrive pacing
    3. non-selective BB
    4. lidocaine if refractory
214
Q

How should stable, sustained VT be managed?

A

Stable sustained VT = >30sec

  1. DC cardioversion vs Procainamide
  2. IV amio
  3. Lidocaine
215
Q

What is an electrical storm and how is it managed?

A
  • Def: ≥3 episodes in 24 hrs
  1. Beta-blockers, preferably non-selective
  2. IV amio
  3. Consider sedation / anesthesia
  4. Consult heart rhythm expert early
  5. Treat acute HF if present
216
Q

What investigations should be considered in patients with VT/VF

217
Q

What is the Brugada algorithm to differentiate VT and SVT in wide complex tachycardia?

218
Q

What is the Vereckei algorithm to differentiate VT and SVT in wide complex tachycardia?

219
Q

How would you decide if a patient presenting to the ER with syncope requires admission

220
Q
A
  1. Cardiac testing based on high suspicion of ischemic, structural or valvular disease
  2. Stress testing in all presenting with syncope before, during or after exertion
  3. Brain imaging if IC disease is highly suspected or head trauma
  4. No carotid imaging unless focal
  5. Tilt table test if Dx uncertanty
    1. Atypical presentation
    2. older patient with few Hx clues
    3. distinguishing convulsive syncope vs epilepsy
    4. non-HD collapse
221
Q

What type of at home monitoring is appropriate for patients with ?arrhythmic syncope based on their Sx frequency?

222
Q

How are vasovagal syncopes managed?

A
  1. Education/reassurance
  2. avoid triggers
  3. Increased H2O and Na+
  4. Counterpressure maneuvers
  5. Fludrorcortisone
  6. Midodrine
  7. BB (age >42)
223
Q

How is syncope 2/2 orthostatic hypotension managed?

A
  1. Education
  2. Avoid triggers
  3. Increased H2O + Na
  4. Medication review
  5. Compression garments
  6. Head-up tilt sleeping
  7. Fludrocortisone
  8. Midodrine
224
Q

When should PPM be considered in Vasovagal syncope

A
  1. Patients ≥40 with highly symptomatic VVS
  2. Documented symptomatic asystole >3s
  3. Documented asymptomatic asystole >6s
  4. Tilt induced asystole >3s or HR <40 for >10s
225
Q

What are the driving restrictions after PPM insertion?

A
  1. Private
    1. 7 days
  2. commercial
    1. 1 month
    2. Document normal ECG after
226
Q

What are the driving restrictions after ICD insertion

A
  • Private
    • Primary prophylaxis
      • 1 month
    • Secondary prophylaxis
      • 6 months
  • Commercial
    • No driving for life
227
Q

What are the driving restrictions after VT/VF with no reversible cause?

A
  1. Private
    1. 6 months
  2. Commercial
    1. NO driving
228
Q

What are the driving restrictions after AF or SVT

229
Q

What are the driving restrictions after medically treated AS, MS, MR, AI

A
  • Private
    • AS
      • OK to drive if NYHA 1-2 and no syncope
    • MS-MR-AI
      • NYHA 1-2 and no syncope OK
  • Commercial
    • AS
      • OK to drive if NYHA1, EF≥35%, AVA ≥1
    • MS, MR, AI
      • NYHA 1, EF≥35%
230
Q

What are the driving restrictions after vasovagal syncome

A

can drive as long as not provoked while sitting, typical vasovagal

231
Q

What are the driving restrictions after recurrent unexplained syncope

A
  1. Private
    1. 3 months symptom-free
  2. commercial
    1. 12 months symptom-free
232
Q

What are the driving restrictions in NYHA I CHF

A
  1. Private
    1. No restrictions
  2. Commercial
    1. OK if EF>35
233
Q

What are the driving restrictions in NYHA II CHF

A
  1. Private
    1. No restrictions
  2. Commercial
    1. OK if EF>35
234
Q

What are the driving restriction in NYHA III CHF

A
  1. Private driving
    1. No restrictions
  2. Commercial
    1. No driving
235
Q

What are the driving restriction in NYHA IV CHF, patients with LVADs or patients on inotropes

A
  1. NO DRIVING
236
Q

What is POTS and how is it diagnosed?

A
  1. Postural orthostatic tachycardia syndrome (orthostatic tachycardia without hypotension)
    1. Orthostatic intolerance (sustained increased HR >30bpm supine within 10 mins of standing with no drop in BP 20/10)
      1. R/O secondary causes (hypovolemia, thyroid, etc…)
      2. R/O systemic disease (ehler danlos, autoimmune neuropathy)
237
Q

What symptoms are associated with POTS

A
  1. Palpitations
  2. chest dyscomfort
  3. lightheadedness
  4. chronic fatigue
  5. chronic pain
  6. Nausea
238
Q

What workup should be sent for POTS if the diagnosis is not clear

A
  1. Basic labs
    1. CBC
    2. Lytes
    3. Cr
    4. TSH
    5. AM cortisol
  2. No need for specialized cardiac testing
239
Q

What are the non-pharmacological management strrategies in POTS

A
  1. Exercise training
  2. Na 10g/day
  3. H2O 3-4L/day
  4. Waist-high compression stockings
240
Q

What are the pharmacological treatment options in POTS?

A
  1. Midodrine
  2. Fludrocortisone
  3. Other weaker recomendations
    1. Ivabradine
    2. Methyldopa
    3. Clonidine
241
Q

How should cardiovascular risk be assessed in competitive athletes?

A
  1. Get conset for screening
  2. Start with Hx & P/E
  3. No routine screening. ECG only if concerning features
242
Q

What should be considered in competitive athletes with conditions putting them at risk for SCD?

A
  1. Sport restriction
243
Q

If an S3 or S4 is present, where can it most commonly be heard?

A

LLSB or apex

244
Q

Which murmurs increase with inspiration?

A
  1. Right sided murmurs
245
Q

Which murmurs increase with expiration?

A

Left siided murmurs

246
Q

Which P/E maneuvers increase venous return?

A
  • Leg raise
  • Squat
247
Q

Which P/E maneuvers increase afterload

248
Q

Which P/E maneuvers decrease afterload?

A

Amyl nitrate

249
Q

What happens to AS murmurs with increased venous return

250
Q

What happens to AS murmurs with increased afterload

251
Q

What happens to MS murmurs with increased venous return

A

Louder (same as AS)

252
Q

What happens to MS murmurs with increased afterload

A

Softer (Same as MS)

253
Q

What happens to MR murmurs with increased venous return

254
Q

What happens to MR murmurs with increased afterload?

255
Q

What happens to AR murmurs with increased venous return

256
Q

What happens to AR murmurs with increased afterload

A

Louder (same as MR)

257
Q

What happens to HOCM murmurs with increased venous return

A

Softer (opposite of AR/MR)

258
Q

What happens to HOCM murmurs with increased afterload

259
Q

What happens to MVP murmurs increased venous return?

260
Q

What happens to MVP murmurs with increased afterload

A

Softer (opposite of MR, AR)

261
Q

What conditions can cause a systolic and regurgitant murmur

262
Q

If a systolic and regurgitant murmur is accompanied by respiratory variations and a large V wave, what pathology does this suggest?

263
Q

If a systolic and regurgitant murmur is accompanied by a non-elevated JVP, what pathology does this suggest?

A

chronic MR

264
Q

If a systolic and regurgitant murmur is accompanied by a displaced apex, what pathology does this suggest?

A

Chronic MR

265
Q

If a systolic and regurgitant murmur is accompanied by an elevated JVP but no respiratory variation, CHF and a normal apex, what pathology does this suggest?

266
Q

If a systolic and regurgitant murmur is accompanied by a click, what pathology does this suggest?

A

MR with MVP

267
Q

If a systolic and regurgitant murmur radiates from the LSB to the RSB, what pathology does this suggest?

268
Q

What conditions can cause a systolic ejection murmur/mid or late peaking?

A
  1. Aortic stenosis
  2. Aortic sclerosis
  3. HOCM
269
Q

If a systolic ejection murmur radiates to the carotid is accompanied by diminished carotid pulse and maybe an apical carotid delay, what pathology does this suggest?

270
Q

If a systolic ejection murmur is accompanied by a double carotid pulse, a ‘triple ripple’ apical beat, a non-displaced apex, and a superimposed MR murmur what pathology does this suggest?

271
Q

If a systolic ejection murmur has no features of AS or HOCM, what pathology does this suggest?

A

Aortic sclerosis

272
Q

What can cause a low pitch rumbling diastolic murmur?

A
  1. MS
    1. consider functionnal MS
273
Q

What is an austin flint murmur

A

Murmur of AI with functional MS

274
Q

If a low pitch rumbling diastolic murmur is accompanied by an opening snap after S2 that is usually best head at the apex, what pathology does this suggest?

275
Q

What causes a higher-pitched diastolic murmur

276
Q

If a diastolic murmur is best heard at the RUSB, what pathology doses this suggest?

277
Q

What should you also check for on P/E when you hear a murmur suggestive of AR?

A
  1. Signs of pHTN
  2. Signs of a dilated LV
  3. Austin flint murmur at the apex
  4. Widened pulse pressures
278
Q

How does an AR murmur evolve as the severity of the valvulopathy gets worst

A

It becomes shorter (ends quicker)

279
Q

What causes an S3 (S4 can also be present)

A
  1. CHF/Biventricular failure
280
Q

What causes an S4 alone

A
  1. Stiff LV
    1. HTN
    2. HFpEF
281
Q

What causes a scratching sound with more than 2 components on cardiac auscultation?

A

Pericardial rub

282
Q

What causes a continuous murmur through systole and diastole?

A
  1. PDA
  2. Coarctation
  3. Ruptured sinus of Valsalva to atrium
  4. Aortopulmonary window
  5. Internal mammary artery (mammary soufle)
  6. Venous hum in jugular (stops with pressure)
  7. Arterial stenosis (i.e. sublcavian)
  8. Any AV fistula
    1. AVM
283
Q

What can cause a loud S1

A
  1. Short PR
  2. Exercise
  3. Increased transvalvular flow
    1. ASD
    2. PDA
  4. AV valve obstruction
    1. MS
    2. TS
284
Q

What can cause a soft S1

A
  1. Calcific MS
  2. MR
  3. early closure of the valve
    1. Long PR
    2. AI
    3. LBBB
285
Q

What can cause a variable S1

A
  1. AF
  2. AV dissociation
  3. Severe tamponade
286
Q

What can cause a wide split S1

A
  1. RBBB
  2. ASD
  3. Ebstein’s anomaly
287
Q

What can cause a loud A2?

A
  1. Severe HTN
  2. CoA
  3. Aneurysm
288
Q

What can cause a Loud P2

A

Pulmonary HTN

ASD

289
Q

What can cause a soft A2?

A
  1. AI
  2. Severe calcific AS
290
Q

What can cause a soft P2?

A
  1. Low PAP
  2. PS
291
Q

What can cause a wide split S2?

A
  1. RBBB
  2. LV PPM
292
Q

What can cause a wide fixed S2?

A
  1. ASD
  2. RV failure
293
Q

What can cause a paradoxically split S2?

A
  1. LBBB
  2. WPW
  3. fixed LVOT
  4. AS
  5. HOCM
294
Q

What P/E findings are most specific to rule in AS?

A
  1. Slow rate of rise of carotid pulse (+LR 2.8-130)
  2. mid to late peak of murmur (+LR 8-100)
  3. Soft S2 (+LR 3-50)
295
Q

What P/E exam findings can help R/O AS?

A

Absence of radiation to the R carotid (-LR 0.05-0,1)

296
Q

List the risk factors for sudden death in HOCM

A
  1. Family history of SCD
  2. spontaneous sustained VT
  3. VF cardiac arrest
  4. unexplained syncope
  5. LV thickness ≥ 30mm (low PPV)
  6. Abnormal exercise BP, NSVT

Other minor RF that may be considered in individual cases

  1. MI
  2. AS
  3. Competitive exertioon
  4. High-risk mutation
  5. LV outflow obstruction (>30mm)
297
Q

How can AS and HOCM be differentiated on physical exam?

298
Q

What are the physical exam findings in ASD

A
  1. Wide fixed split S2
  2. Don’t usually hear a murmur
    1. Possible to hear diastolic rumble from increased flow through TV or a pulmonary ejection murmur
299
Q

What are the physical exam findings in VSD

A
  1. Holosystolic murmur 3rd-4th ICS with thrill
  2. Smaller defects generate louder murmurs
300
Q

What is the best physical exam test to both rule in and rule out tamponade?

A
  1. Pulsus paradoxus
301
Q

What physical exam tests, other than pulsus paradoxes, can help rule out tamponade if absent

A
  1. Tachycardia
  2. elevated JVP
302
Q

What physical exam findings are surprisingly not helpful in tamponade

A
  1. Hypotension
  2. diminished heart sounds
303
Q

In what conditions can a pulsus paradoxus be found?

A
  1. Tamponade
  2. Severe asthma (or exaggerated inspiratory efforts)
  3. RV infarct
  4. PE
  5. Severe pectus excavatum
  6. Severe asthma/COPD
304
Q

What physical exam tests help rule in PAD in patients with symptoms?

A
  1. Discoloration (LR+2.8)
  2. Pulse abnormality in symptomatic leg (LR+4.7)
  3. Bruit in symptomatic leg (LR+5.6)
  4. Symptomatic leg cooler to touch (LR+5.9)
  5. Wounds or sores (LR+5.9)
305
Q

What physical exam tests help rule out PAD in patients with symptoms?

A

Absence of any pulse abnormality

306
Q

What physical exam tests help rule in PAD in patients with no symptoms

A
  1. Any pulse abnormality (LR+3)
  2. Presence of femoral bruit (LR+4.8)
307
Q

What physical exam tests help rule out PAD in patients with no symptoms?

A

none particularily robust, absence of pulse abnormality is best

308
Q

Describe an arterial ulcer

A
  1. punched out on toes and feet
309
Q

Describe a venous stasis ulcer

A

medial calf

310
Q

Where is a diabetic foot ulcer usually found

A

plantar foot

heel

311
Q

In patients with an unpalpable dorsal pedis pulse, what do you expect to find

A

palpable posterior tibialis

312
Q

List 3 “special tests” in PAD

A
  1. Venous filling time
    1. Empty vein by elevating to 45 deg for 1 minute, then patient sit up
    2. Mesure time of duration from return of vein from collapsed state
    3. >20 sec is abnormal
  2. Capillary refil
    1. 5 sec of pressure to skin of distal great toe
    2. > 5sec for color to return is abnormal
  3. Buerger’s test
    1. Elevate leg to 90deg with patient suppine for 2 min
    2. Dangle leg perpendicular to table edge for 2 min
    3. Positive test=palor with elevation, dusky rubor with dependancy
313
Q

What is the non-pharmacological therapy for PAD

A
  1. Exercise
  2. Self-foot exam
  3. Wound care
314
Q

What is the pharmacological therapy for PAD?

A
  1. ASA or clopidogrel in symptomatic PAD
    1. Can also be reasonable in asymptomatic patients
    2. As per COMPASS: can consider ASA + Riva 2.5
  2. ACE for all patients, also treat HTN as per guideline
  3. Smoking cessation
  4. DM treatment
  5. Cilostazol (PDE3 inh. – selective, quinolone derivative) effective to improve symptoms and increase walking distance
    1. *CI in CHF patients
  6. Anticoagulation (IV heparin) for acute limb ischemia
  7. Statin in all

*CI: Anticoagulation solely for PAD, pentoxifylline, prostanoids, chelation therapy

315
Q

What are the indications for surgical revascularisation in PAD

A
  1. Life limiting claudication with inadequate response to OMT
  2. Critical limb ischemia

RCPSC (14 decks)

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