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BPT > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Aortic stenosis indices

A

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

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2
Q

MR and AR indices

A

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

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3
Q

Causes of AS + percentages in people <70

A

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

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4
Q

Causes of AS + percentages in people >70

A

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

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5
Q

AS murmur

A

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

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6
Q

AS other findings

A

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

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7
Q

AS indications of severity

A

Late peaking, longer duration of murmur, soft S2

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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
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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
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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

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11
Q

AR murmur

A

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

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12
Q

What is the Austin Flint murmur

A

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

Associated with AR

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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

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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)

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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
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16
Q

MS murmur

A

Diastolic rumble loudest on expiration (duration correlates with severity)

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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
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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)

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19
Q

Complications of MS

A
  • Chronic or paroxysmal AF : 45%
  • Systemic thromboembolic events: 13-26%
  • Functional TR
  • pHTN *indicator of bad outcomes
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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

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21
Q

MS medical + interventional management

A

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

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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

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23
Q

MR other signs

A

Soft S1, early A2, loud S3

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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

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25
Q

TR murmur

A

Pansystolic murmur (louder on inspiration)

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26
Q

MS in pregnancy

A

Severe MS often become symptomatic, even if ok pre-pregnancy. Manage with bed rest, beta blocker and consider valvuloplasty after 20 weeks

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27
Q

PS murmur

A

ESM loudest on inspiration

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28
Q

Flecainide – MoA, indications, CI, AE

A

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

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29
Q

Beta blockers – MoA, indications, CI, AE

A

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

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30
Q

Amiodarone – MoA, indications, CI, AE

A

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%)

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31
Q

Verapamil – MoA, indications, CI, AE

A

MoA: CCB
Indications: AF, prophylaxis of pSVT, multifocal atrial tachycardia
AE: AV block, HF, constipation, flushing, oedema

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32
Q

Adenosine – MoA, indications, CI, AE

A

MoA: transient AV nodal block via activation of Gi proteins
Indications: SVT
AE: chest pain, hypotension, flushing, bronchospasms, sense of impending doom

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33
Q

Digoxin – MoA, indications, CI, AE

A

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

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34
Q

What are the features of WPW

A

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
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35
Q

ACE inhibitor

A

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

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36
Q

Dihydropyridine CCB - amlodipine

A

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
Q

Thiazides

A

MoA: block Na/Cl symporter in distal tubules
Indications: HTN, hypercalciuria
AE: new onset diabetes in <65 years, hyponatraemia

38
Q

Alpha blockers - prazocin

A

MoA: alpha1 selective antagonists reduces peripheral vasoconstriction and resistance
Indications: men w both BPH + HTN
AE: postural hypotension, increase rate of CV events

39
Q

Aldosterone antagonists - spironolactone

A

MoA: mineralocorticoid receptor antagonist
Indications: add on for resistant HTN
AE: hyperkalaemia, AKI

40
Q

Essential HTN management

A

Initial therapy: ACEi or ARB + CCB or diuretic
Step 2: ACEi or ARB + CCB + diuretic
Step 3: add spironolactone, alpha or beta blocker

41
Q

Essential HTN management in CAD

A

Initial therapy: BB + either ACEi / ARB / CCB / diuretic
Step 2: triple combination of above
Step 3: add spironolactone, alpha or beta blocker

42
Q

Essential HTN management in CKD

A

Initial therapy: ACEi / ARB + CCB / diuretic
Step 2: ACEi / ARB + CCB + diuretic
Step 3: add spironolactone, alpha or beta blocker

43
Q

Betablocker

A

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
Q

ACEi

A

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
Q

ARNI - entresto (sacubitril / valsartan)

A

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
Q

Ivabradine

A

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
Q

Digoxin

A

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
Q

Furosemide

A

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
Q

Spironolactone

A

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
Q

Statins

A

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
Q

Ezetimibe

A

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
Q

PCSK9 (Evolocumab, alirocumab)

A

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
Q

Fenofibrate

A

MoA: acts on the perioxisome proliferator activated receptor
Indications: high triglycerides, low HDL
AE: abdominal pain ,deranged LFTs

54
Q

Familial hyperlipidemia pathophysiology

A

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
Q

Lipid profile in hypothyroidism

A

High LDL

56
Q

Lipid profile in DM

A

High triglycerides

57
Q

Lipid profile in excess alcohol

A

High LDL, low triglycerides

58
Q

Statin myopathy clinical presentation

A

Symptoms start weeks - months after commencing therapy. Characterised by fatigue, muscle pain, weakness, nocturnal cramping, distribution is proximal, generalised and worse with exercise

59
Q

Statins with less muscle toxicity

A

Pravastatinandfluvastatin

60
Q

Lipid targets

A

Primary prevention with high CVD risk: LDL <2

Secondary CVD prevention: LDL <1.8

61
Q

Secondary causes of high LDL + total cholesterol

A
  • Dietary
  • OCP/HRT
  • Hypothyroidism
  • Nephrotic syndrome
  • CLD/PBC
62
Q

Secondary causes of high triglycerides

A
  • Dietary
  • Medications: thiazodes/isoretinoin/steroids/HAART/OCP/HRT
  • Diabetes
  • Hypothyroid
  • Pregnancy
63
Q

Secondary causes of low HDL

A
  • Diet/obesity
  • Smoking
  • Diabetes
64
Q

Indications for TTE

A

Prior MI, SSx of heart failure, undiagnosed murmur, complex ventricular arrhythmia
To assess LVEF

65
Q

Indications for angiography

A
  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
Q

Pharmacological therapy: medications and benefits

A

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
Q

Prevent IHD progression

A
  • 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 considerSGLT2 inhibitors and GLP1 receptor agonists
  • F/U every 6-12/12 with detailed history, blood glucose and lipid profile and ECG, influenza vaccine
68
Q

Indications for revascularisation (PCI or CABG) over medical therapy

A
  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
Q

Management of single vessel disease

A

PCI with drug-eluting stent

70
Q

Management of two vessel disease involving right and circumflex coronary arteries

A

PCI with drug-eluting stents

71
Q

Management of two vessel disease involving left anterior descending + right main or circumflex

A

CABG in pt with diabetes or large amount of myocardium supplied by diseased vessel

72
Q

Management of triple vessel disease

A

CABG, unless low SYNTAX score and non-diabetic

73
Q

Stent thrombosis timings

A

Acute = 24 hr
Subacute = 24hr to 30d
Late = 30d-1 year
Very late = >1 year

74
Q

Peripheral vascular disease - 6 ps

A

Paraesthesia, pain, pulselessness, poikilothermia (cool), pallor, paralysis

75
Q

ABI values and toe pressure values to diagnose PVD

A

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
Q

Brugada syndrome ECG changes

A

Pseudo RBBB and persistent ST elevation in V1 - V3 (coved or saddle-back

77
Q

Arrhythmogenic Right Ventricular Dysplasia (ARVD) ECG changes

A
  • 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
Q

Long QT syndrome ECG findings

A

QTc >450ms for men, >470ms for women

79
Q

Medications that prolong QTc

A
  • 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
Q

Management of torsades de pointe

A
  1. IV magnesium
  2. Temporary overdrive pacing with aim HR 100
  3. Isoprenaline
  4. IV lignocaine
81
Q

Indications for AAA repair

A

Asymptomatic + size >5.5cm or symptomatic

82
Q

Indications for bridging clexane

A
  • 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
Q

Aortic dissection Daily system

A

Type A: involve the ascending aorta (ascending twice as common as descending)
Type B: everything else

84
Q

Aortic dissection clinical triad

A

Abrupt onset tearing/ripping thoracic/abdominal pain + variation in pulse or blood pressure (>20mmHg) + widening of mediastinum on CXR

85
Q

Aortic dissection management

A
  1. Aim HR <60 w BB
  2. Aim SBP 100 with GTN
  3. Surgical review -> type A is cardiac surgical emergency
86
Q

BP target in DM

A

<140/90

87
Q

BP target for patients <65

A

<130/90

88
Q

Indications to start treatment for hypertension

A

> 140/90 or >130/85 in high risk patients (CAD)

BPT (3 decks)

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