Cardiology Flashcards

1
Q

Aortic stenosis indices

A

Vmax > 4m/s, Valve area < 1.0cm2, DVI < 0.25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MR and AR indices

A

Regurgitant fraction of > 50%, Regurgitant volume > 60mLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of AS + percentages in people <70

A

50% bicuspid, 25% post-inflammatory and 18% degenerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of AS + percentages in people >70

A

48% degenerative, 27% bicuspid, 23% post-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AS murmur

A

ESM, loudest right 2nd intercostal space, mid-clavicular line, radiating to carotids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

AS other findings

A

Carotid upstroke, soft/reversed split S2, S4 if SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AS indications of severity

A

Late peaking, longer duration of murmur, soft S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is low flow, low gradient AS

A
  • Low cardiac output state (HF, especially HFrEF)
  • Leads to underestimation of severity of disease
  • Dobutamine stress echo helps to differentiate between pseudo AS and true AS by increasing cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Indications for AS treatment

A
  1. Symptomatic
  2. Asymptomatic but undergoing other cardiac surgery
  3. Asymptomatic but LVEF <50% or BP drop with exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is AVR preferred to TAVI in patients <60 years

A

Risks of paravalvular leak, PPM requirements, future coronary access, complicated redo procedure and durability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

AR murmur

A

Early diastolic murmur, heard best sitting up, on full expiration at L sternal edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the Austin Flint murmur

A

Low-pitched, mid to late diastolic rumble, heard at the apex

Associated with AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs of wide pulse pressure

A

§ Corrigan pulse/waterhammer pulse/collapsing pulse

Traube’s sign = pistol shot pulse - systolic and diastolic sounds, heard over the femoral arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Frequency of AR monitoring based on severity

A

Mild: 3-5 years
Moderate 1-2 years
Severe: 0.5-1 year
Clinical stages of chronic AR are defined by symptoms, valve anatomy, severity of regurgitation, and LV systolic function (LVEF and LV dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Indications for AR intervention

A
  • symptomatic AR, severe AR or asymptomatic severe AR with LV dilation
  • 55/55/55 rule: LVEF <55%, LV end systolic diameter >55mm, LV end systolic volume >55ml/m
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MS murmur

A

Diastolic rumble loudest on expiration (duration correlates with severity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MS other signs

A

Pulmonary hypertension - mitral facies (pink/purple patches on the cheeks), parasternal heave, palpable S2

  • Right ventricular failure
  • JVP: prominent ‘a’ wave (absent in AF), prominent ‘v’ wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TTE findings of MS

A

Domed/hockey stick appearance of mitral valve, thickened/calcified subvalvular apparatus, LA enlargement, commissural fusion (fish mouth valve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Complications of MS

A
  • Chronic or paroxysmal AF : 45%
  • Systemic thromboembolic events: 13-26%
  • Functional TR
  • pHTN *indicator of bad outcomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Indications for MS intervention

A

Symptomatic + severe MS (MVA <1.5cm2, MG >10mmHg)
Asymptomatic + pHTN / AF / recurrent embolic events on anticoagulation / undergoing intermediate to high risk non-cardiac surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MS medical + interventional management

A

1st line: percutaneous valvulotomy - needs favourable valve, no LA thrombus,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MR murmur

A

Systolic murmur radiated to axilla (anterior leaflet disease) or to sternum (posterior leaflet disease)
- Little respiratory variation - louder with handgrip/squatting due to increased venous return, softer with valsalva or standing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MR other signs

A

Soft S1, early A2, loud S3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Primary MR indications for intervention

A

Indications
- Symptomatic
- Asymptomatic + LV <60%, LVESD >40mm, AF, pHTN
Relative indications
- Likelihood repair >95% with mortality <1%
- Progressive LV changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
TR murmur
Pansystolic murmur (louder on inspiration)
26
MS in pregnancy
Severe MS often become symptomatic, even if ok pre-pregnancy. Manage with bed rest, beta blocker and consider valvuloplasty after 20 weeks
27
PS murmur
ESM loudest on inspiration
28
Flecainide – MoA, indications, CI, AE
MoA: sodium channel blocker Indications: chemical cardioversion, maintenance of SR in AF, last resort for VT Contraindication: post AMI / structural heart disease as worsen HF AE: prescribe with AV nodal blocking agent as can lead to 1:1 conduction
29
Beta blockers – MoA, indications, CI, AE
MoA: decreases SA + AV node activity, prolongs AV node repolarisation, slows conduction velocity Indications: AF rate control, paroxysmal SVT, atrial / ventricular premature beats, ventricular arrhythmias CI: acute heart failure AE: exacerbation of COPD/asthma, sedation/CNS depression
30
Amiodarone – MoA, indications, CI, AE
MoA: potassium channel blocker, inhibitsdelayed potassium channels –> prolongs repolarisation Indications: AF *most effective for pAF AE: – Pulmonary fibrosis and infiltrates – Thyroid dysfunction: hypothyroidism most common – Liver dysfunctio: raised AST/ALT (15–50%), hepatitis/cirrhosis (<3%) – Neurological (tremor/peripheral neuropathy/ataxia) – GIT (nausea/anorexia/constipation) – Photosensitivity (25–75%) – Corneal microdeposits (>90%)
31
Verapamil – MoA, indications, CI, AE
MoA: CCB Indications: AF, prophylaxis of pSVT, multifocal atrial tachycardia AE: AV block, HF, constipation, flushing, oedema
32
Adenosine – MoA, indications, CI, AE
MoA: transient AV nodal block via activation of Gi proteins Indications: SVT AE: chest pain, hypotension, flushing, bronchospasms, sense of impending doom
33
Digoxin – MoA, indications, CI, AE
MoA: increases contractility and decreases HR by inhibiting Na/K ATPases Indication: AF, HF AE: nausea/vomiting, abdominal pain, blurred vision with yellow tint and halos
34
What are the features of WPW
Refers to the presence of a congenital accessory pathway and episodes of tachyarrhythmias - PR interval <120ms - Delta wave, upsloping of initial part of QRS - QRS prolongation > 110ms - ST-segment and T-wave discordant changes - May mimic posterior infarction
35
ACE inhibitor
MoA: blocks conversion of angiotensin 1 to 2 -> reduces arterial vasoconstriction, reduced aldosterone, reduces water and Na reabsorption Indications: HF, post-MI, proteinuria AE: hyperkalaemia, AKI, dry cough (build up of bradykinin), angioedema
36
Dihydropyridine CCB - amlodipine
MoA: selectively blocks voltage gated Ca channels on arterial smooth muscles Indications: HTN, angina, SAH, raynaud's AE: reflex tachycardia (at higher doses), vasodilation- oedema, flushing, dizziness, gingival hypertrophy
37
Thiazides
MoA: block Na/Cl symporter in distal tubules Indications: HTN, hypercalciuria AE: new onset diabetes in <65 years, hyponatraemia
38
Alpha blockers - prazocin
MoA: alpha1 selective antagonists reduces peripheral vasoconstriction and resistance Indications: men w both BPH + HTN AE: postural hypotension, increase rate of CV events
39
Aldosterone antagonists - spironolactone
MoA: mineralocorticoid receptor antagonist Indications: add on for resistant HTN AE: hyperkalaemia, AKI
40
Essential HTN management
Initial therapy: ACEi or ARB + CCB or diuretic Step 2: ACEi or ARB + CCB + diuretic Step 3: add spironolactone, alpha or beta blocker
41
Essential HTN management in CAD
Initial therapy: BB + either ACEi / ARB / CCB / diuretic Step 2: triple combination of above Step 3: add spironolactone, alpha or beta blocker
42
Essential HTN management in CKD
Initial therapy: ACEi / ARB + CCB / diuretic Step 2: ACEi / ARB + CCB + diuretic Step 3: add spironolactone, alpha or beta blocker
43
Betablocker
MoA: negative chronotropic effect, slows HR Indications: all HF patients CI: 2nd / 3rd degree heart block, do not start during decompensated HF AE: bradycardia, hypotension
44
ACEi
MoA: inhibits conversion of angiotensin 1 to 2 Indications: all HR patients CI: bilateral renal artery stenosis, pregnant / breastfeeding AE: dry cough, hyperkalaemia, angioedema,
45
ARNI - entresto (sacubitril / valsartan)
MoA: neprolysin inhibitor Indications: replacement for ACEi/ARB when on maximal dose or beta-blocker and ACEi (mortality benefit CI: cease ACE 36/24 prior to commencing AE: renal impairment, hypotension, hyperkalaemia
46
Ivabradine
MoA: Selective inhibitor of cardiac pacemaker If current that controls spontaneous diastolic depolarisation in the sinus node and regulates heart rate Indications: EF <35% and SR with HR >70 with maximum dose of ACEi and beta-blocker CI: 3rd degree AV block, acute HF, AMI AE: luminous phenomena, bradycardia
47
Digoxin
MoA: reversibly inhibit the alpha subunit of sodium potassium ATPase -> positive ionotropic effects Indications: ongoing NYHA class II, III, and IV symptoms despite optimal therapy CI: VT/VF known accessory pathway, 3rd degree AV block AE: visual disturbances, N/V, diarrhoea Toxicity: arrhythmia and conduction disturbances, PVC
48
Furosemide
MoA: inhibit sodium and chloride absorption in the ascending limb of loop of Henle’s and in both proximal and distal tubule Indications: fluid overload CI: ESKD, hypokalaemia AE: headache, dizziness, dry mouth, dehydration, hypovolaemia, hypocalcemia, hyponatremia
49
Spironolactone
MoA: aldosterone antagonist, competitive binding of receptors at aldosterone dependent sodium potassium site in distal convoluted tubule. Indications: all patients with EF <40% - spironolactone has evidence to decrease proteinuria in combination with ACEi and ARB CI: hyperkalaemia, Addison's disease, AKI AE: gynaecomastia, lethargy, maculopapular/erythematous cutaneous eruption, agranulocytosis, change in libido, SJS/TENS
50
Statins
MoA: HMG-CoA reductase inhibitor, blocks conversion of HMG-CoA to mevalonate, the rate-limiting step of cholesterol biosynthesis Indications: predominant hypercholesterolemia, secondary prevention in ischaemic stroke CI: pregnancy / breastfeeding AE: myopathy, rhabdomyolysis, new onset diabetes and haemorrhagic stroke
51
Ezetimibe
MoA: partially inhibits intestinal cholesterol absorption, targets jejunal enterocyte brush border cholesterol transport protein Nieman Pick C1 like 1 protein Indications: in combination with statin, as alternative to statin AE: nausea, diarrhoea, drowsiness
52
PCSK9 (Evolocumab, alirocumab)
MoA: Increases LDL receptors on the liver and thus increasing LDL up take by the liver by blocking PCSK9 enzyme that degrades LDL receptor Indications: In Australia is subsidised for patients with familial hyperlipidaemia not meeting LDL targets with atorvastatin, simvastatin or ezetimibe AE: well tolerated
53
Fenofibrate
MoA: acts on the perioxisome proliferator activated receptor Indications: high triglycerides, low HDL AE: abdominal pain ,deranged LFTs
54
Familial hyperlipidemia pathophysiology
Inheritance - Homozygous: 10 fold increase of cholesterol, presents with ACS at 20 years - Heterozygous: 3-4 fold, presents with ACS at 30-40 years Pathophysiology: - ApoB 3500 mutation , LDL-R gene**most common, PCSK9 gene and apolipoprotein B gene AKA apoB3500 - Phenotype is extremely elevated LDL-C and early onset artherosclerotic disease - Clinical signs: tendinous xanthamata **most specific
55
Lipid profile in hypothyroidism
High LDL
56
Lipid profile in DM
High triglycerides
57
Lipid profile in excess alcohol
High LDL, low triglycerides
58
Statin myopathy clinical presentation
Symptoms start weeks - months after commencing therapy. Characterised by fatigue, muscle pain, weakness, nocturnal cramping, distribution is proximal, generalised and worse with exercise
59
Statins with less muscle toxicity
Pravastatin and fluvastatin
60
Lipid targets
Primary prevention with high CVD risk: LDL <2 | Secondary CVD prevention: LDL <1.8
61
Secondary causes of high LDL + total cholesterol
- Dietary - OCP/HRT - Hypothyroidism - Nephrotic syndrome - CLD/PBC
62
Secondary causes of high triglycerides
- Dietary - Medications: thiazodes/isoretinoin/steroids/HAART/OCP/HRT - Diabetes - Hypothyroid - Pregnancy
63
Secondary causes of low HDL
- Diet/obesity - Smoking - Diabetes
64
Indications for TTE
Prior MI, SSx of heart failure, undiagnosed murmur, complex ventricular arrhythmia To assess LVEF
65
Indications for angiography
1. Initial test in resuscitated sudden cardiac arrest 2. Life-threatening ventricular arrhythmias 3. Symptoms and signs of heart failure 4. Results of non-invasive testing indicate high likelihood of severe disease 5. LVEF <50 and moderate risk on non-invasive testing 6. Inconclusive/contraindications to non-invasive testing Unsatisfactory QoL with angina
66
Pharmacological therapy: medications and benefits
1st line: betablocker -> reduce anginal episodes, improve ET, prevents re-infarction + improves survival in patient with previous MI/LV dysfunction 2nd line: calcium channel blocker -> increases coronary and peripheral vasodilation and reducing contractility 2nd line: long-acting nitrates improves exercise tolerance by reducing pre-load and afterload 3rd line/other: Ranolazine, late sodium channel blocker, nicorandil (potassium channel activator, veno/arterial dilator), perhexiline (inhibition of fatty acid oxidisation, hepato/neurotoxicity)
67
Prevent IHD progression
- Aspirin - Statin - ACEi or ARB in patients with hypertension, diabetes, LVEF <40% or CKD (proteinuric) - Lifestyle modifications: smoking cessation, weight reduction and glycaemic control  - For patients with diabetes consider SGLT2 inhibitors and GLP1 receptor agonists  - F/U every 6-12/12 with detailed history, blood glucose and lipid profile and ECG, influenza vaccine
68
Indications for revascularisation (PCI or CABG) over medical therapy
1. Patients with activity limiting symptoms despite maximal medical therapy 2. Active patients who want PCI to improve their QoL or if they are not tolerating medical therapy well 3. Patients with anatomy where revascularisation has a proven survival benefit - Left main coronary artery disease (>50% luminal narrowing) - Multivessel coronary artery disease with reduced LVEF and a large area of potentially ischaemic myocardium
69
Management of single vessel disease
PCI with drug-eluting stent
70
Management of two vessel disease involving right and circumflex coronary arteries
PCI with drug-eluting stents
71
Management of two vessel disease involving left anterior descending + right main or circumflex
CABG in pt with diabetes or large amount of myocardium supplied by diseased vessel
72
Management of triple vessel disease
CABG, unless low SYNTAX score and non-diabetic
73
Stent thrombosis timings
Acute = 24 hr Subacute = 24hr to 30d Late = 30d-1 year Very late = >1 year
74
Peripheral vascular disease - 6 ps
Paraesthesia, pain, pulselessness, poikilothermia (cool), pallor, paralysis
75
ABI values and toe pressure values to diagnose PVD
ABI <0.9 = diagnostic of PAD ABI <0.4 = diagnostic of critical limb ischaemia ABI >1.4 indicates presence of calcified non-compressible arteries, uninterpretable for PAD - Next step is to calculate toe pressures or toe-brachial index - Toe pressure <40mmHG or toe-brachial index <0.7 is diagnostic of PAD
76
Brugada syndrome ECG changes
Pseudo RBBB and persistent ST elevation in V1 - V3 (coved or saddle-back
77
Arrhythmogenic Right Ventricular Dysplasia (ARVD) ECG changes
- Monomorphic VT with LBBB pattern - QRS V1 >110 seconds - Epsilon wave (m in S wave) *most specific, seen in 50% of pts - TWI V1-3
78
Long QT syndrome ECG findings
QTc >450ms for men, >470ms for women
79
Medications that prolong QTc
- Antiarrhythmics: sotalol* (esp. in renal impairment) > amiodarone (rarely associated with TdP), quinidine - Psychotropic drugs: haloperidol, methadone, risperidone, clozapine, TCA, SSRIs - Ondansetron - Antibiotics: macrolide, azoles, anti-malarials, quinolone, metronidazole - Anti-histamines
80
Management of torsades de pointe
1. IV magnesium 2. Temporary overdrive pacing with aim HR 100 3. Isoprenaline 4. IV lignocaine
81
Indications for AAA repair
Asymptomatic + size >5.5cm or symptomatic
82
Indications for bridging clexane
- Mechanical heart valve: MVR, stroke/TIA <6/12 ago - AF: CHADsVASC greater than or equal to 5, stroke <3/12 ago, rheumatic valvular heart disease - VTE: high risk thrombophilia, VTE <3/12 ago
83
Aortic dissection Daily system
Type A: involve the ascending aorta (ascending twice as common as descending) Type B: everything else
84
Aortic dissection clinical triad
Abrupt onset tearing/ripping thoracic/abdominal pain + variation in pulse or blood pressure (>20mmHg) + widening of mediastinum on CXR
85
Aortic dissection management
1. Aim HR <60 w BB 2. Aim SBP 100 with GTN 3. Surgical review -> type A is cardiac surgical emergency
86
BP target in DM
<140/90
87
BP target for patients <65
<130/90
88
Indications to start treatment for hypertension
>140/90 or >130/85 in high risk patients (CAD)