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Cardiology > Cardiology part 6 > Flashcards

Cardiology part 6 Flashcards

1
Q

Peripheral Artery Disease (PAD)

A

x

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2
Q

syx

A

x

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3
Q

what are the syx of PAD?

A

claudication (pain with exertion), rest pain, tissue ulceration, gangrene

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4
Q

pathophys

A

x

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5
Q

what is the pathophys of PAD?

A

atherosclerotic narrowing that most commonly occurs toward the proximal end of large peripheral arteries (eg, iliac, popliteal)

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6
Q

risk

A

x

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7
Q

what are risk factors for PAD?

A

smoking, DM, HTN, advancing age

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8
Q

trx

A

x

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9
Q

what is the best trx for PAD?

A

aspirin, <=75y.o. should also get a high intensity statin (40-80mg daily atorvastatin, 20-40 mg daily rosuvastatin)

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10
Q

what is sometimes used for syx improvement, if lifestyle modifications (ie excercise, smoking cessation) have failed?

A

cilostazol (PDE3 inhibitor)

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11
Q

stepwise treatment of symptomatic PAD

A

x

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12
Q

what is step 1A of treatment?

A

Risk factor management: smoking cessation, BP and diabetes control, antiplatelet and statin therapy

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13
Q

what is step 1B of treatment?

A

supervised excercise therapy (30-45 minutes of supervised walking >=3 times a week for >3 months, then gradually increase walking periods)

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14
Q

what is step 2 of treatment?

A

cilostazol BID (preferred over pentoxifylline)

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15
Q

what is step 3 of treatment?

A

revascularization for persistent symptoms:

  • angioplasty +/- stent placement
  • autogenous or synthetic bypass graft
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16
Q

Dressler Syndrome (post cardiac injury syndrome)

A

x

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17
Q

pathophys

A

x

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18
Q

what is the pathophys of dressler syndrome?

A

immune mediated pericarditis that can occur several weeks following an MI

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19
Q

timing

A

x

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20
Q

when does Dressler Syndrome usually occur?

A

several weeks following MI

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21
Q

Ventricular Aneurysm

A

x

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22
Q

cause

A

x

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23
Q

when does ventricular aneurysm typically occur?

A

as a late complication typically weeks to months after acute MI

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24
Q

dx

A

x

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25
Q

what are the characteristic EKG findings?

A

persistent ST elevation, along with deep Q waves in the same leads

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26
Q

pathophys

A

x

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27
Q

what isthe usual pathohpys of ventricular aneurysm?

A

left ventricular enlargement causing heart failure, refractory angina, ventricular arrythmias, or systemic arterial embolization from mural thrombus

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28
Q

Coronary Revascularization (CABG)

A

x

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29
Q

indications

A

x

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30
Q

what are indications for CABG in patients with stable angina?

A
  • Patients with refractory angina despite maximal medical therapy
  • Patients in whom revascularization will improve long-term survival. This includes those with left main coronary stenosis and those with multivessel CAD (especially involving the proxima
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31
Q

in patients with multivessel CAD (especially involving the proximal LAD) and LVD, what should you do?

A

CABG more superior than PCI with drug eluting stent

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32
Q

management

A

x

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33
Q

patients with multivesel CAD and DM would benefit from what?

A

CABG more superior than PCI with drug eluting stent

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34
Q

PCI with bare or metal eluting stents

A

x

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35
Q

indications

A

x

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36
Q

when is PCI with bare or metal eluting stents an excellent revaascularization option?

A

for patients with refractory angina due to severe single or two vessel CAD not involving the proximal LAD

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37
Q

Ranolazine

A

x

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38
Q

what is the purpose of ranolazine?

A

antianginal agent (reduce the frequency and severity of anginal syx in patients with refractory symptoms on conventional medical therapy with nitrates, beta blockers, and/or calcium channel blockers.)

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39
Q

Bicuspid Aortic Valve

A

x

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40
Q

epid

A

x

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41
Q

what is typical gender for bicuspid aortic valve?

A

affects 1% of population

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42
Q

association

A

x

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43
Q

what disease is it associated with?

A

30% of turner syndrome patients

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44
Q

genetics

A

x

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45
Q

what is the genetic pattern?

A

autosomal dominant with incomplete penetrance or sporadic

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46
Q

dx

A

x

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47
Q

how do you diagnose it?

A

screening echocardiogram for patient and 1st degree relatives

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48
Q

what does CXR show?

A

unremarkable but occasionally shows AV calcification, aortic enlargement (due to aneurysm), or rib notching (due to coarctation)

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49
Q

complications

A

x

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50
Q

what are the complications of bicuspid aortic valve?

A

infective endocarditis, severe regurgitation or stenosis, aortic root or ascending aortic dilation, dissection

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51
Q

what is the specific condition that these patients should be evaluated for?

A

thoracic aortic aneurysm

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52
Q

management

A

x

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53
Q

what should do for follow up of bicuspid aortic valve?

A

f/u echo every 1-2 years

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54
Q

what other managment options are there for bicuspid aortic valve?

A

balloon valvuloplasty or surgery (valve and ascending aorta replacement)

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55
Q

Balloon valvuloplasty is indicated in symptomatic and asymptomatic (if they plan to become pregnant or participate in competitive sports) young adults when the following criteria are met:

A
  • aortic stenosis
  • no significant AV calcification or aortic regurgitation
  • peak gradient > 50 mm Hg
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56
Q

PE

A

x

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57
Q

what are physical exam findings?

A

2/6 midsystolic murmur is heard at the left sternal border

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58
Q

screening

A

x

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59
Q

first degree relatives should be screened for what?

A

screen for bicuspid AV to avoid complications of severe regurg, stenosis, ascending aorta or aortic root dilation, and dissection

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60
Q

Acute Coronary Syndrome (ACS)

A

x

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61
Q

risk

A

x

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62
Q

what are risks for ACS?

A

smoking, DM, HTN, HLD, fam hx

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63
Q

which risk factor is considered most significant for adverse cardiovascular outcomes?

A

Diabetes Mellitus (especially in women), hence why it is considered a CHD risk equivalent.

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64
Q

why does strict glycemic Diabetes Mellitus control still lead to complications of CHD and stroke?

A

strict control significatnly lowers microvascular complications (eg retinopathy nephropathy, neuropathy) but does not consistently reduce macrovascular complications (eg CHD, stroke)

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65
Q

in addiition , CHD risk factors including ___, ___, ___ have synergistic effects with DM and greatly increase the risk.

A

HTN, Smoking, Obesity

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66
Q

what are CHD risk equivalents?

A
  • noncoronary atherosclerotic disease (eg carotid, PAD, AAA)
  • DM
  • CKD
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67
Q

what are CHD established risk factors ?

A
  • age (especially >50 yo in men and menopause in women)
  • male gender
  • Fam Hx of CHD in 1st degree relative <50 y.o. in men or <60 y.o. in women
  • HTN (<140/90 for diabetics)
  • HLD
  • Smoking hx (especially if >=1 pack/day)
  • Obesity
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68
Q

syx

A

x

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69
Q

what are syx suggestive of ACS?

A

anginal pain lasting longer than 20 minutes

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70
Q

what are syx suggestive of Angina?

A

stable angina syx usually resolves within a few minutes of rest or sublingual nitroglycerin

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71
Q

Dx

A

x

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72
Q

what inital test would be done?

A

EKG, trops

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73
Q

how often do EKGs show MI?

A

nondiagnostic or normal in 1/2 of MI’s

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74
Q

how often do trops elevate after MI?

A

top levels remain undetectable for 6-12 hours following onset of syx

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75
Q

what does EKG finding concerning for ACS show?

A

ST segment depression in II, III, aVF and V3-V6

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76
Q

what are other EKG findings concnerning for CAD?

A

T wave abnormalities in leads II, III, aVF

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77
Q

managment

A

x

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78
Q

what is the most appriorpriate approach to patients with ACS but normal EKG and trops?

A

serial EKG and trop levels (eg, 3 troponin levels 6 hours apart and several ECGs 30 minutes apart)

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79
Q

in patients with low risk non ST elevation MI or unstable angina based on TIMI score, what tests could be performed?

A

pharm stress echo and excercise radionuclide perfusion scan are stress tests that allow for the identification of myocardial regions that have inducible ischemia

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80
Q

when do you do a cardiac catheterization?

A
  • STEMI w HD instability

- NSTEMI (do it within 24-48 hours)

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81
Q

Unstable Angina and NSTEMI

A

x

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82
Q

syx

A

x

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83
Q

what are syx of Unstable Angina and NSTEMI?

A

x

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84
Q

risk

A

x

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85
Q

what are risk factors for Unstable Angina and NSTEMI?

A

x

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86
Q

ddx

A

x

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87
Q

what is the ddx for Unstable Angina ?

A

pneumothorax, pulmonary embolism, aortic dissection, NSTEMI, STEMI

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88
Q

workup

A

x

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89
Q

what orders for Unstable Angina and NSTEMI should be placed stat?

A

oxygen, BP monitoring, IV access, cardiac monitoring, and EKG.

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90
Q

what meds for Unstable angina should be placed STAT?

A

Aspirin

Nitroglycerin (as long as BP can tolerate)

Beta blocker (goal HR 60-70), IV morphine (when the chest pain is not immediately relieved with NTG or when acute pulmonary congestion and/or severe agitation is present)

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91
Q

what is next tests to order for distinguishing NSTEMI and Unstable Angina?

A

cardiac enzymes

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92
Q

what are other orders that should be placed in addtion to cardiac enzymes?

A

CBC, BMP, PT/INR, PTT, LFTs, CXR, and Echo

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93
Q

distinction

A

x

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94
Q

how do you distinguish NSTEMI and Unstable Angina?

A

CK-MB and troponin should be checked, do serial cardiac enzymes (2 sets 8 hours aparat)

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95
Q

if you have elevated CK-MB and troponins, what does that suggest, Unstable Angina or NSTEMI?

A

NSTEMI

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96
Q

if you have normal CK-MB and troponins, what does that suggest, Unstable Angina or NSTEMI?

A

Unstable Angina

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97
Q

initial management

A

x

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98
Q

what is the initial management for Unstable Angina and NSTEMI?

A

IV heparin, as long negative FOBT

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99
Q

what is another initial management for Unstable Angina and NSTEMI?

A

beta blocker to bring the heart to 60-70bpm

100
Q

what high risk features make a person a candidate for early invasive therapy in unstable angina or NSTEMI?

A

refractory ischemia, recurrent syx, ST segment depression (as in this patient), and hemodynamic instability.

101
Q

the presence of unstable angina with high risk features is an indication for early invasive therapy so what should be orderd?

A

early invasive therapy and angiography, so cardiology consult and catheterization are indicated.

102
Q

the presence of unstable angina is an indication for early invasive therapy , especially if ST depression are present, catheterization is indicated and what medication should be added?

A

GP IIB/IIIA inhibitors (clopidogrel, eptifibatide)

103
Q

further management

A

x

104
Q

what is the first step in management of Unstable Angina/NSTEMI?

A

TIMI RIsk score

105
Q

what should all NSTEMI patients be treated with?

A

1) dual antiplatelet therapy with ASA and Platelet P2Y12 receptor blockers (clopidogrel, prasugrel, or ticagrelor)
2) Nitrates
3) Beta Blockers
4) Statins
5) Anticoagulant therapy (unfractioned heparin, LMWH, bivalirudin, fondaparinux)

106
Q

dx

A

x

107
Q

what are ekg findings conerning for unstable angina?

A

T wave inversions in lead V5-V6, ST depression

108
Q

how do you most often diagnose Unstable Angina?

A

largely by history (syx of angina without elevated cardiac biomarkers)

109
Q

management

A

x

110
Q

what is the management of unstable angina and NSTEMI?

A

nitrates (use w cuation in hypotension i.e. right ventricular failure), beta blockers, antiplatelet therapy, anticoagulation, statin therapy, coronary reperfusion

111
Q

which of the previously listed meds is contraindicated in heart failure and bradycardia?

A

beta blockers

112
Q

when using nitrates in NSTEMI and UA, what should you worry about ?

A

caution with hypotension (eg right ventricular infrarction)

113
Q

when using beta blockers in NSTEMI and UA , which ones should you use?

A

cardioselective (eg metoprolol, atenolol), IV hypertensive patients

IV beta blockers for HTN patients

114
Q

when using antiplatelet therapy in NSTEMI and UA , which ones should you use?

A

aspirin and P2Y12 receptor blockade (eg clopidogrel)

115
Q

when using statin therapy in NSTEMI and UA , which ones should you use?

A

high intensity (eg atorvastatin, rosuvastatin) with a goal of LDL <=50mg/dL

116
Q

if there is intolerance to high intensity statin, what should be done?

A

every other day dosing, reduction of statin intensity (pravastatin)

117
Q

when using coronary reperfusion in NSTEMI and UA , when should you do it?

A

PCI within 24 hours.

118
Q

final management

A

x

119
Q

once cardiac cath is complete in UA or NSTEMI, what is next?

A

risk reduction (lipid profile, TSH-if dyslipidemia present, smoking cessation, cardiac diet-low sodium and cholesterol), excercise program, discharge medications (aspirin, beta blocker, statin, and sublingual nitro, clopidogrel)

120
Q

TIMI Score (Thombolysis in Myocardial Infarction Risk Score)

A

x

121
Q

indications

A

x

122
Q

when is TIMI score indicated to be used?

A

for managment of unstable angina/non ST elevation myocardial infraction

123
Q

how it’s used

A

x

124
Q

how do you use the TIMI score?

A

1 point for each of the following:

  • age >=65
  • > = 3 risk factors for CAD (age, HLD, HTN, DM, fam hx, etc)
  • known CAD with >50% stenosis
  • use of aspirin in the past 7 days
  • > =2 anginal episodes within the preceding 24 hours
  • elevated serum cardiac biomarkers (eg troponin I)
  • ST segment deviation >0.5mm on admission EKG
125
Q

what categories exist for each TIMI score?

A
  • low risk (0-2) do a stress test;
  • intermediate or high (3-7) risk do early coronary angiography w/n 24 hours;
  • HD instability, Heart failure or new MR, reccurrent CP, ventricular arrhythmia do immediate coronary angiography
126
Q

Sudden Cardiac Death (SCD)

A

x

127
Q

pathophys

A

x

128
Q

what is the pathophys of SCD?

A

ventricular arrhythmias triggered by intense exertion in the setting of undiagnosed structural heart disease (HOCM, AAOCA, Arrythmogenic right ventricular cardiomyopathy)

129
Q

epid

A

x

130
Q

what is the epidemiology of SCD?

A

most common cause of athletes <35 y.o.

131
Q

Athlete’s Heart

A

x

132
Q

pathophys

A

x

133
Q

what makes athletes have bradycardia?

A

intense training have a heightened vagal tone that often results in heightened vagal tone resulting in bradycardia w or w/o first degree AV block

134
Q

dx

A

x

135
Q

what is the EKG finding of athletes heart?

A

LV wall thickness that meets voltage criteria for LVH . Prolonged PR interval (consistent with first degree AV block)

136
Q

managmeent

A

x

137
Q

what is the managemetn for athletes heart?

A

reassurance

138
Q

syx

A

x

139
Q

what is the syx of athletes heart?

A

slow heartbeat

140
Q

when do you use 24 hour EKG montioring ?

A

patients with unexplained syx (eg palpitaitons, syncope)

141
Q

Chronic Heart Failure (CHF)

A

x

142
Q

heart failure stages

A

x

143
Q

there are how many stages of heart failure?

A

Stages A-D

144
Q

Stage A heart failure is?

A

high risk heart failure without structural heart disease or heart failure symptoms

145
Q

Stage B heart failure is?

A

structural heart disease, but without signs or syx of heart failure (patients with prior MI or valvular heart disease with LV enlargement or low EF)

146
Q

Stage C heart failure is?

A

structural heart disease without prior or current syx of heart failure

147
Q

Stage D heart failure is?

A

heart failure syx at rest or refractory end stage heart failure

148
Q

dx

A

x

149
Q

how do you dx CHF?

A

echo showing regional wall abnormalities (suggest ischemia) or significant valvular abnormalities

150
Q

how to most patients with ischemic cardiomyopathy present? what are next steps that should be taken for work up?

A

many patients with ischemic cardiomyopathy do not have typical anginal symptoms and initially present with symptoms of heart failure (eg dyspnea, volume overload). Therefore those who are asyx should be evaluated for CAD with stress testing or Coronary angio

151
Q

what does BNP help with distinguishing in regards to heart failure?

A

help differentiate heart failure exacerbation from other causes of dyspnea, just like trops help with detection of myocardial necrosis and infraction

152
Q

trx

A

x

153
Q

what should all patients with asyx LVSD be treated with?

A

ACE inhibitor (delay onset of syx heart fialure and improve long term cardiac morbidity and mortality)

154
Q

what other trx should be given to CHF patients beside ACE inhibitors?

A

beta blocker

155
Q

what do you give for syx LVSD (left ventricular systolic dysfxn)?

A

digoxin, spiranolactone

156
Q

in patients with ischemic cardiomyopathy, they often have reversibly depressed contractility. What is an important intervention that must be taken?

A

coronary revascularization , which can lead to improvment in symptoms, systolic function, and long term mortality

157
Q

Pulmonary Hypertension (pHTN)

A

x

158
Q

classificaitons

A

x

159
Q

how do you classify pHTN?

A

into groups; there are 5 groups each due to a specific cause

160
Q

what is group 1 pHTN due to?

A

idiopathic pulmonary arterial HTN

161
Q

what is group 2 pHTN due to?

A

left sided heart disease (PCWP >18 mmHg)

162
Q

what is group 3 pHTN due to?

A

chronic lung disease (COPD, ILD)

163
Q

what is group 4 pHTN due to ?

A

chronic thormboembolic disease

164
Q

what is group 5 pHTN due to?

A

other causese (eg sarcoidosis, OSA)

165
Q

syx

A

x

166
Q

what are the symptoms of pHTN?

A

PROGRESSIVE dyspnea, fatigue/weakness, exertional angina, syncope, abdominal distention/pain

167
Q

PE

A

x

168
Q

what are physical exam findings?

A
  • Left parasternal lift, right ventricular heave
  • Loud P2, right-sided S3
  • Pansystolic murmur of tricuspid regurgitation
  • Right heart failure: JVD, ascites, peripheral edema, hepatomegaly
169
Q

dx

A

x

170
Q

what does CXR characteristically show?

A

enlargmeent of the main pulmonary arteries with attenuation of peripheral arteries

171
Q

what does EKG show?

A

NSR with right axis deviation

172
Q

what is intial eval of pHTN?

A

transthoracic echo

173
Q

what is definitve diagnostic test for pHTN?

A

right heart cath with mean pulmonary arterila pressure >=25 mm Hg

174
Q

what measurement rules out pHTN due to left heart failure?

A

PCWP <18 mmHg

175
Q

trx

A

x

176
Q

what is the goal of trx for pHTN?

A

treat underlying cause

177
Q

what is the trx for group 1 pHTN (i.e idiopathic pulm HTN)?

A

endothelin receptor antagonists-to dilate pulmonary arteries

178
Q

what are other trx options for idiopathic PAH?

A

PDE-5 inhibitors (eg sildenafil, tadalafil) and prostracyclin pathway agonists (eg epoprostenol, treprostinil, iloprost)

179
Q

what is the trx for group 2 pHTN (i.e Left sided Heart disease)?

A

ARBs (-artans)

180
Q

what is the trx for group 3 pHTN (i.e chronic lung disease)?

A

muscarinic antagonists (ipratroprium, tiotropium) for trx of COPD

181
Q

Acute Arterial Occlusion

A

x

182
Q

PE

A

x

183
Q

what are the physical exam findings of acute arterial occlusion?

A

acute onset pain, diminished pulses, paleness, coolness

184
Q

if you have an acute arterial occlusion with a apical diastolic murmur, what is the likely cause?

A

atrial myxoma

185
Q

pathophys

A

x

186
Q

what is the pathophys of acute arterial occlusion?

A

embolus from a proximal source, acute thrombosis of an atherosclerotic plaque, or direct trauma to the involved artery

187
Q

cause

A

x

188
Q

what is the cause of acute arterial occlusion?

A

afib, severe ventricular dysfunction, endocarditis, valvular disease, atrial myxoma, or a prosthetic valve

189
Q

Atrial Myxoma

A

x

190
Q

epid

A

x

191
Q

what are the most common primary cardiac tumors?

A

atrial myxomas

192
Q

presentation

A

x

193
Q

the tumors can be large enough where they present how?

A

mitral vavle obstruction (diastolic murmur and tumor plop), rapidly worsening heart failure, new onset afib

194
Q

dx

A

x

195
Q

how is the diagnosis made?

A

echocardiography (TEE better than TTE)

196
Q

trx

A

x

197
Q

what is the treatment of atrial myxoma?

A

prompt surgical excision

198
Q

Factor V Leiden

A

x

199
Q

complications

A

x

200
Q

what are you increased risk of?

A

increased risk of venous thrombosis (eg deep, cerebral, or mesenteric venous thrombosis)

201
Q

Deep Vein Thrombosis or Pulmonary Embolism (DVT or PE)

A

x

202
Q

trx

A

x

203
Q

how long do you anticoag patients with DVT or PE for patients who do not have cancer?

A

> =3 months

204
Q

what are the two mainstay trx options?

A

warfarin and oral factor Xa inhibitors

205
Q

for patients with an underlying malignancy who develop DVT or PE, what is more efficacious , LMWH or Factor Xa inhibitors?

A

LMWH

206
Q

do you use antiplatelets in trx of DVT or PE?

A

no

207
Q

oral factor Xa inhibitors (i.e. rivaroxaban)

A

x

208
Q

what is MOA?

A

direct factor Xa inhibition

209
Q

what is the therapeutic onset?

A

2-4 hours

210
Q

is there bridging/overlap required?

A

no

211
Q

is there lab monitoring required?

A

no

212
Q

warfarin

A

x

213
Q

what is MOA?

A

vitamin K antagonism

214
Q

what is the therapeutic onset?

A

5-7 days

215
Q

is there bridging/overlap required?

A

yes, overlap with UFH or LMWH for ~5 days

216
Q

is there lab monitoring required?

A

Prothrombin time/INR

217
Q

Menopausal Hormone Therapy (MHT)

A

x

218
Q

complications

A

x

219
Q

what are complications of MHT?

A

stroke, breast cancer, VTE

220
Q

purpose

A

x

221
Q

what is the purpose of MHT?

A

treatment of hot flashes (>80% of perimenopausal and early menopausal women)

222
Q

Hot Flashes

A

x

223
Q

trx

A

x

224
Q

what is the most effective way to treat women with VTE while on MHT who are worried about getting hot flashes after stopping MHT?

A

SSRIs (eg escitalopram) and SNRIs (venlafaxine) are very effective (50%-70% of women reduce such symptoms)

225
Q

what medication is a breast cancer trx for postmenopausal women that has estrogenic effects on bones and antiestrogenic effects on breast and uterus? does it raise or lower hot flash risk ?

A

raloxifene, increases risk of hot flashes

226
Q

Aortic Regurgitation

A

x

227
Q

PE

A

x

228
Q

what is a classic PE finding of Aortic regurg?

A

wide pulse pressures

229
Q

Aortic Stenosis (AS)

A

x

230
Q

syx

A

x

231
Q

what are the syx of Aortic Stenosis?

A

syncope while working, fatigability

232
Q

PE

A

x

233
Q

what are the physical exam findings of AS?

A
  • carotid pulses are delayed
  • harsh crescendo decrescendo murmur heard at the base of the heart
  • second heart sound is soft with an inaudible A2 component
234
Q

what are the physical exam findings of severe AS?

A
  • soft, single second heart sound (S2) during inspiration/absence of physiological splitting of S2
  • a delayed and diminished carotid pulse (‘ parvus et tardus’)
  • loud and late peaking systolic murmur
235
Q

what is the pathophys of severe AS heart sounds ?

A

during inspiration normally , you have increased blood in right side of the heart that results in delayed closure of the pulmonic valve and earlier closure of the aortic vavle causing a split of aortic valve (A2) and pulmonic valve (P2) components of S2.

in severe AS, closure of the aortic valve is delayed , which results in nearly simultaneous closure of the aortic and pulmonic valves during inspiration, and is appreciated as a single S2 (or even paradoxical, with A2 noticeable after P2).

236
Q

what physical exam is suggestive of mild to moderate AS?

A

early peaking AS murmur (relatively low left ventricular pressure attain early in ventricular systole is needed to overcome the valvular stenosis)

237
Q

what is the associated heart sound with blood filling a dilated ventricle is ____, what is the associated heart sound with blood filling a concentric LVH and decreased wall compliance____

A

S3, S4

238
Q

dx

A

x

239
Q

what does EKG show?

A

LVH, secondary ST segment and T wave changes

240
Q

what does Echo show?

A

LVH with severe calcification of the aortic valve

241
Q

how do you define severe aortic stenosis on echo?

A

aortic jet velocity >=4.0 m/sec
-or-
mean tranvavlvular gradient >=40 mm Hg

-either of which typically occurs with aortic valve area decreases to <=1 cm2.

242
Q

management

A

x

243
Q

what are indications for valve replacement?

A

severe aortic stenosis and >=1 of the following:

  • onset of syx (eg angina, syncope)
  • LVEF< 50%
  • undergoing other cardiac surgery (eg CABG)
244
Q

when do you do percuteaneous balloon aortic vavlulotomy?

A

considered only as a bridge to surgical or transcatheter aortic valve replacemetn in patients with severe syx AS

245
Q

should you use diuretics or vasodilators in those with severe AS?

A

no these patietns are preload dependent

246
Q

mortality

A

x

247
Q

what is average survival of people with severe AS without valve replacemetn?

A

2-3 years

Cardiology (7 decks)

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