Cardiology Flashcards

1
Q

What is the MOA of Sacubitril?

A
  • Neprilysin inhibition
  • Neprilysin is an enzyme that degrades atrial and brain natriuretic peptides (ANP, BNP), bradykinin and adrenomedullin which are endogenous vasodilating peptides.
  • Sacubitril therefore increases the levels of these peptides.
  • Antihypertensive effect:
    1. reduce blood volume
    2. increased sodium excretion
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2
Q

Sacubitril-valsartan improves outcomes in HFREF (heart failure with reduced ejection fraction) compared to Enalapril. What are these outcomes (3)?

A
  1. Reduced cardiac death and hospitalisation for HF
  2. Reduced overall mortality
  3. Reduced symptoms and improved function

Summary: improved morbidity, mortality and symptoms

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3
Q

Combining ACEi and Neprolysin inhibition (sacubutril) leads to what serious complication?

A

Serious angioedema - therefore sacubitril is combined with ARB.

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4
Q

T/F: continuous infusion of epoprostenol (Flolan) improves the survival of patient with pulmonary arterial hypertension.

A

True.

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5
Q

What is epoprostanol?

A
  • drug version of Prostacyclin (aka Prostaglandin I2)

- potent vasodilator and inhibits platelet activation

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6
Q

Post ACS, addition of which drug to statin therapy improves cardiovascular outcomes?

A

Ezetimibe

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7
Q

T/F: Obesity is an independent risk factor for AF

A

True

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8
Q

What ECG signs are suggestive of dextrocardia?

A
  1. Tall R-wave in V1

2. Absent R-wave in V6

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9
Q

Patient has ECG findings suggestive of dextrocardia and reports being infertile, what is the diagnosis

A

Dextrocardia + Infertility = Kartagner’s syndrome

Infertility is due to ciliary dyskinesia

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10
Q

Transmission of which pathogen is peculiar to cardiac transplant from the donor heart compared to other solid organ transplants?

A

Toxoplasma gondii.

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11
Q

What % of patients with HFREF have central sleep apnoea?

A

15%

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12
Q

How is ‘severe’ aortic stenosis defined according to the following parameters:

  1. VA: Valve area (cm^2) - also, what is considered ‘critical’?
  2. PV: Maximum aortic velocity - aka peak velocity (m/s)
  3. MPG: Mean pressure gradient (mmHg)
A
  1. VA less than 1 (critical is less than 0.6) cm^2
  2. PV more than 4 m/s
  3. MPG more than 40 mmHg
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13
Q

In the medical treatment of HOCM, what drugs are recommended and which should be avoided?

Name 2 of each.

A

Recommended:
1st line - beta blockers
2nd line - verapamil (non-dihydropyridine CCB)

Avoid (may worsen LVOT obstruction):

  • GTN (vasodilators)
  • Frusemide (diuretics)
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14
Q

T/F: Most cardiac tumours are benign.

A

True (75% benign)

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15
Q

What is the most common type of cardiac tumour?

Where is it usually located?

A
  • Myxomas (mesenchyme origin) that are capable for neural and endothelial differentiation.
  • 80% found in the left atrium, the rest in the right atrium.
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16
Q

What is the clinical significance of a positive parasternal heave?

A

Suggests RV-hypertrophy, rarely left atrial enlargement pushing RV forward.

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17
Q

What are the 2 clinical pre-cordial findings of pulmonary HTN?

A
  1. Parasternal heave - RV-hypertrophy

2. Palpable P2 (i.e. P2 tap) - closure of PV

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18
Q

In the Stress ECG test, which of the following is more specific for myocardial ischaemia:

  1. Upsloping ST depression
  2. Horizontal ST depression
  3. Downsloping ST depression
A

Horizontal and downsloping is more specific

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19
Q

What specific ECG finding on a Stress ECG test is considered ‘positive’ for myocardial ischaemia?

A

Great than or equal to 1 mm horizontal/downsloping ST depression in one or more leads that persists at 80 milliseconds after the J point.

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20
Q

What are 6 ECG end-points on a Stress ECG test that should prompt termination of the test?

A

Ischaemia:
1. Marked ST depression

Arrhythmias:

  1. New BBB
  2. VT or VF
  3. Increasing ventricular ectopy
  4. SVT
  5. HB (Mobitz II or CHB)
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21
Q

What are 3 types of ventricular ectopy?

A
  1. Premature beats
  2. Couplets
  3. NSVT
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22
Q

What mechanism creates the ‘ultra’ sound in the ultrasound probe?

A
  • Striking of piezo-electrical crystals with an electric pulse.
  • Crystals release sound waves
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23
Q

With ultrasonography, what is the relationship of the frequency of the ultrasound and resolution and tissue penetration?

A

Increased frequency leads to INCREASED resolution but DECREASED tissue penetration.

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24
Q

For the E/A ratio of cardiac ultrasound (pulse-wave doppler across the MV), what is the significance of the E-wave and A-wave?

Is the ratio positive or negative under normal conditions?

A

E-wave (early wave) = passive filling of the ventricle
A-wave (atrial wave) = active filling with atrial systole

Normally, E-wave is slightly greater than A-wave, therefore E/A ratio is usually POSITIVE.

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25
Q

REVERSAL of the E/A ratio (i.e. negative value) in cardiac doppler is due to which process (give 4 potential causes)?

A

Decrease LV compliance.

4 examples: old age, HTN, LVH, diastolic dysfunction

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26
Q

EXAGGERATION of the E/A ration (i.e. more positive) in the cardiac doppler is due to which process (give 3 potential causes)?

A

Decrease in LV compliance.

3 examples: restrictive cardiomyopathy, contrictive pericarditis, infiltrative cardiac disease (e.g. amyloidosis)

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27
Q

What is the classic ECG finding with Digoxin toxicity?

A

Reverse tick sign - downsloping ST depression

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28
Q

Describe the mechanism behind the type of arrhythmia that Digoxin toxicity causes.

A

Increased automaticity (increased intracellular calcium) and decreased AV conduction (increased vagal effects at the AV node) leads to:

  • SVT: due to increased automaticity
  • Slow ventricular response: due to decreased AV conduction

i.e. ’atrial tachycardia with block’.

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29
Q

What is the MOA of Ezetimibe?

What are the 2 main AEs?

A

Lowers cholesterol by decreasing the absorption of cholesterol in the small intestines.

AEs: steatorrhoea and headache

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30
Q

Does high or low calcium levels cause prolongation of the QT interval and hence increase risk of torsade de pointes.

A

Hypocalcaemia causes prolonged QT

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31
Q

For each of the following options:

  1. Troponin
  2. Myoglobin
  3. CK-MB

Match to the most appropriate comments:

  • first to rise post-MI
  • returns to normal after 2-3 days
  • remains elevated for 10d
A
  1. Troponin - remains elevated for 10d
  2. Myoglobin - first to rise post-MI
  3. CK-MB - returns to normal after 2-3 days
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32
Q

What is the most common cause of sudden cardiac death in the young patient?

A

HOCM

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33
Q

In a normotensive 13 week pregnant women with a previous history of pre-eclampsia. What medication will decrease the risk of recurrence?

A

low-dose aspirin

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34
Q

What is the most common cause of ‘cyanotic’ congenital heart disease at birth or in the first few days?

A

Transposition of the Great Arteries (TGA) is the most common cause in neonates.

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35
Q

What is the most common cause of ‘cyanotic’ congenital heart disease in general?

A

Tetralogy of Fallot (occurs 1-2 months after birth)

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36
Q

What is the most common cause of ‘acyanotic’ congenital heart disease?

A

Ventricular Septal Defect (VSD)

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37
Q

What is the anatomical abnormality in patent ductus arteriosus?

A

Connection between the pulmonary trunk and descending aorta

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38
Q

T/F: Patent ductus arteriosus is a CYANOTIC congenital heart defect.

A

False - acyanotic.

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39
Q

Describe the murmur of a patent ductus arteriosus in terms of the following:

  1. Character of murmur
  2. Location of murmur
  3. Associated pulse character
  4. Associated features (2)
A
  1. Character of murmur: continuous ‘machinery’ murmur
  2. Location of murmur: left sternal edge (subclavicular)
  3. Associated pulse character: collapsing pulse
  4. Associated features (2):
    - Widened pulse pressure
    - Heaving apex beat
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40
Q

For following phases (0-4) of the cardiac action potential, describe the flux of electrolytes.

0 - rapid depolarisation
1 - early repolarisation
2 - plateau
3 - final repolarisation
4 - restoration
A

0 - rapid depolarisation
- rapid INFLUX of sodium

1 - early repolarisation
- EFFLUX of potassium

2 - plateau
- EFFLUX of potassium in balance with slow INFLUX of calcium

3 - final repolarisation
- EFFLUX of potassium

4 - restoration

  • Resting potential (-96mV) restored by Na+/K+ ATPase (Na+ out and K+ in)
  • Na+ slowly enters until threshold potential reached triggering a new action potential
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41
Q

T/F: skeletal remains contracted longer than cardiac muscle.

A

False - cardiac muscle remains contracted 10-15x longer than skeletal muscles.

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42
Q

What is the conduction velocity (m/s) in the following regions of the heart:

  1. Atrium
  2. AV-node
  3. Ventricle
A
  1. Atrium = 1 m/s (slow)
  2. AV-node = 0.05 m/s (fastest)
  3. Ventricle = 2-4 m/s (fast)
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43
Q

Regarding congenital ‘coarctation of the aorta’:

  1. What is the anatomical abnormality and what sign does it yield?
  2. Which sex is it more common in?
A
  1. What is the anatomical abnormality?
    - narrowing of the descending aorta leading to radio-femoral delay
  2. Which sex is it more common in?
    Male
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44
Q

Which 4 conditions is ‘coarctation of the aorta’ associated with?

A

2BaNT:

Berry aneurysm
Bicuspid AV
Neurofibromatosis
Turner’s syndrome

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45
Q

What are 6 poor prognostic factors in HOCM?

A

LL-FANS:

Low BP on exercise
LV wall thickness greater than 30mm
FHx of sudden death
Age - young at presentaiton
NSVT on holter monitor
Syncope
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46
Q

Patient with AF has background of WPW. Which of the following medications can be given and which should be avoided?

  1. Digoxin
  2. Flecainide
  3. Metoprolol
  4. Verapamil
  5. Adenosine
A

Inhibiting the AVN may enhance the conduction rate through the accessory pathway, leading to AF becoming VF.

All the following inhibit the AVN:
Digoxin / Metoprolol / Adenosine / Verapamil (worst)

Flecainide is a sodium channel blocker and therefore may be used.

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47
Q

Close of which valves occur in:

  1. S1
  2. S2
A
  1. S1: MV / TV

2. S2: AV / PV

48
Q

Most common cause of S3?

A

LVF

49
Q

What are the 3 causes of S4?

A

Atrial contraction against a stiff ventricle:

AS / HOCM / HTM

50
Q

What is Eisenmenger’s Syndrome?

A

Eisenmenger’s syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension.

51
Q

What are symptom triggers for cessation of an Exercise Tolerance Test (2)?

A
  • Exhaustion

- Severe chest pain

52
Q

What are ECG triggers for cessation of an Exercise Tolerance Test (2)?

A
  • ST depression greater than 3mm

- ST elevation greater than 2mm (or rapid elevation with pain)

53
Q

What are BP triggers for cessation of an Exercise Tolerance Test (2)?

A
  • SBP greater than 230 mmHg

- Fall in SBP greater than >20 mmHg

54
Q

What are HR changes triggers for cessation of an Exercise Tolerance Test (3)?

A
  • Attainment of predicted HR
  • HR fall of greater than 20% of starting HR
  • Arrhythmia
55
Q
Which of the following is NOT a normal variant for an athlete?
•	Sinus bradycardia
•	Junctional rhythm
•	First degree heart block
•	Wenckebach phenomenon
•	LBBB
A

LBBB

56
Q

What are the 5 effects of BNP (B-type natriuretic peptide)?

A
  1. Natriuretic
  2. Diuretic
  3. Vasodilator
  4. Suppresses SNS
  5. Suppresses RAAS
57
Q

Regarding Marfan’s syndrome:

  1. What is the genetic inheritance pattern?
  2. What gene is defective?
  3. How common is it?
A
  1. What is the genetic inheritance pattern? Autosomal Dominant
  2. What is the defect and which gene is defective?
    - Fibrillin-1 gene on chromosome 15
    - Connective Tissue Disorder
  3. How common is it?
    1 in 3000
58
Q

What are the cardiac complications of Marfan Syndrome?

A
  • Dilatation of aortic root (90%)
  • Mitral valve prolapse (75%)
  • Aortic Aneursym / Dissection / Regurgitation
59
Q

When should surgery be consider in a patient with asymptomatic AS?

A

Valvular gradient greater than 40mmHg and LV systolic dysfunction

60
Q

What are the most common causes of AS in the following 2 age groups:

  1. Young patients (below 65 years)
  2. Older patients (above 65 years)
A
  1. Young patients (below 65 years) – biscuspid aortic valve

2. Older patients (above 65 years) – calcification

61
Q

Regarding the following electrolytes, does excess or deficiency cause polymorphic VT:

  1. Calcium
  2. Potassium
  3. Magnesium
    What is the mechanism?
A

Deficits cause polymorphic VT via QT prolongation:

  1. Calcium - hypocalcaemia
  2. Potassium - hypokalaemia
  3. Magnesium - hypomagnesaemia
62
Q

What are the clinical features of severe AS in terms of:

  1. Pulse
  2. BP
  3. Murmur
  4. Heart sounds (2)
  5. Added features (2)
A
1	Pulse – slow rising pulse
2	BP – narrow pulse pressure
3	Murmur – ESM that is late-peaking 
4	Heart sounds (2) – absent/soft S2, S4
5	Added features (2) – systolic thrill over aorta and carotids, LVH (displaces apex beat)
63
Q

In the management of HOCM:

  1. Describe the ABCDE of treatment.
  2. Which 3 drugs should be avoided (AIN)
A
ABCDE:
Amiodarone
Beta-blockers or verapamil
Cardioverting defibrillator
Dual chamber PPM
Endocarditis prophylaxis

AIN: ACEi/ARB, Ionotropes, Nitrates (decrease pre-load)

64
Q

What are the 4 clinical features of TR?

A
  1. PSM loudest in the tricuspid region and on inspiration
  2. Giant V-waves in JVP
  3. Pulsatile liver
  4. Left parasternal heave from RV enlargement
65
Q

Patient is post inferior MI and develops CHB with hypotension.

  1. What is the initial intervention?
  2. When should pacing be considered?
A
  1. What is the initial intervention?
    Atropine and isoprenaline
  2. When should pacing be considered?
    After 7d, if the SR has not resumed then PPM may be considered.
66
Q

Patient is due for an elective cholecystectomy. He has no medical history, is asymptomatic and exams normally. ECG suggests anterolateral ST depression.

Do you:
A. Do further cardiac investigations
B. Do NO further cardiac investigations

A

B. Do NO further cardiac investigations

67
Q

A Doppler probe is placed towards an valve.

What is the direction of blood flow above and below the horizontal axis of the Doppler trace?

A
Above = towards probe
Below = way from probe
68
Q

What are the ABSOLUTE contraindications for TPA in STEMI within the following time frames:

  1. Event(s) occurring now
  2. Event(s) in the last 3m
  3. Event(s) anytime in the past
A

Now:

  • Aortic dissection
  • Active bleed

Last 3m:

  • Ischaemic CVA (unless de novo)
  • Closed head or facial injury

Anytime:

  • Cerebral vascular malformation or malignancy (primary or metastatic)
  • ICH
69
Q

What type of surgery and within what timeframe is a RELATIVE contraindication for TPA in STEMI?

A

Major surgery within the last 3m.

70
Q

What are the time frames for the following 4 major causes of death after cardiac transplantation:

  1. Graft failure
  2. Opportunistic infections
  3. Acute allograft rejection
  4. Cardiac allograft vasculopathy
A

Before 1 year:

  1. Graft failure = within 30 days
  2. Opportunistic infections = 6m to 12m

Before or after 1 year:
3. Acute allograft rejection = after 1 wk to 3yrs

After 1 year
4. Cardiac allograft vasculopathy = after 1 year

71
Q

What is the major cause of death after 5 years of cardiac transplantation?

A

Malignancies (lymphomas and solid tumours)

72
Q

Patient has AF. What type of heart failure (systolic vs. diastolic) would benefit from digoxin for rate-control?

A

Systolic heart failure - LVEF less than 40% after optimisation with ACEi/ARB, BB and diuretics.

73
Q

What is the Sokolov-Lyon criteria (i.e. voltage criteria) for LVH?

A

S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm

74
Q

What is the significance of the following abnormal p-wave morphologies:

  1. Peaked p-wave (p-pulmonale)
  2. Bifid p-wave (p-mitrale)
  3. Inverted p-wave
A
  1. Peaked p-wave (p-pulmonale) = RA enlargement
  2. Bifid p-wave (p-mitrale) = LA enlargement
  3. Inverted p-wave = non-sinus origin of p-wave
75
Q

T/F: Hypotension is a common feature of an acute dissection of the proximal thoracic aorta.

A

False - late presentation due to LVH

76
Q

With the advent of defibrillators in public spaces what is the survival of people with ‘shockable’ rhythms:

A. less than 5%
B. 5-10%
C. 10-20%
D. 20-30%
E. greater then 30%
A

E. greater then 30%

Survival for shockable rhythms = 31% (AHA 2015)

77
Q

What is the clinical syndrome Carney Complex?

A

Carney Complex is a type of MEN (multiple endocrine neoplasms (POTT) - pituitary, ovaries, thyroid, testes.

Associated with skin pigmentation (blue naevi) and cardiac myxomas.

Mutations in the PRKAR1A gene.

78
Q

What is Eisenmenger’s syndrome?

A

Congenital heart conditions (VSD / ASD / PDA) leads to long-term L to R shunt that causes pulmonary HTN, which eventuates in shunt R to L reversal, culminating in cyanosis.

79
Q

What is the normal effect of exercise upon systolic and diastolic BP?

A

SBP becomes rises and DBP remains stable or falls.

80
Q

What finding during a stress exercise ECG test is most predictive of angiographically significant multivessel or left main coronary artery disease?

A

A drop in SBP of greater than 10mmHg from resting BP or failure to increase SBP by 10mmHg.

81
Q

What are the Echocardiographic features of HOCM?

A

‘love MR SAM ASH’

love = LVOT obstruction
MR = Mitral Regurgitation
SAM = Systolic Anterior Motion of mitral valve
ASH = Asymmteric Septal Hypertrophy
82
Q

What are the 2 ECG findings of HOCM?

A
  1. LVH

2. Inferolateral dagger-like Q-waves (II, III, aVF and V5, V6, I, aVL)

83
Q

33% of HOCM are associated with which type of arrhythmia?

A

WPW

84
Q

In a previous normotensive woman, how is pre-eclampsia diagnosed?

A

Diagnosis should be made in a previously normotensive woman with new onset hypertension and proteinuria after 20 weeks of gestation

In the absence of proteinuria, the diagnosis can be made with new onset HTN if associated with end organ dysfunction:

  1. Plts less than 100
  2. Elevated Cr
  3. Deranged LFT
  4. APO
  5. CNS symptoms
85
Q

What is the most COMMON complication of cardiac catheterisation?

A

Arterial false aneurysm (6%) - more likely in femoral approach.

86
Q

What are the most serious complications of cardiac catheterisation?

A
  • Death / MI both 0.1%
  • Stroke 0.5%

All about 1 in 1000

87
Q

List 4 lifestyle changes that lead to reduced BP.

A
  1. Weight loss
  2. Exercise
  3. Diet (decreased EtOH and DASH diet)
  4. Salt restriction
88
Q

What is the DASH diet?

A

In the following order more to less:

  • Grains
  • Fruit and vegetable
  • Low fat dairy
  • Meat
  • Fats / sweet
89
Q

Describe the 6 stages of cardiac myocyte contraction.

A
  1. Cardiac action potential
  2. Ca++ enters cell during the plateau
  3. Ca++ induced Ca++ release from the SR
  4. Ca++ binds to Troponin-C
  5. Cross bridge cycling
  6. Tension
90
Q

How is VO2 Max calculated?

A

VO2 Max = 15.3 x (MHR / RHR)

MHR (Maximum HR ) = 208 - (0.7 x age)
RHR (Resting HR) = HR upon waking up

91
Q

What are 4 ECG features of RVOT tachycardia?

A
  1. QRS > 120ms
  2. LBBB
  3. AV-dissociation
  4. Right or Inferior axis deviation
92
Q

What is lipoprotein (a) (Lp(a)) ?

A
  • LDL + apoB + apo (a) protein

- Lipoprotein (a) is pathogenic and involved coronary heart disease.

93
Q

T/F: conventional lipoprotein lowering drug significantly lower Lp(a) levels.

A

False

94
Q

Lp(a) has strong structural homology to which endogenous molecule?

A

Plasminogen

95
Q

What cardiovascular conditions is elevated Lp(a) levels predictive of?

A
  • Myocardial infarction

- Aortic Stenosis

96
Q

T/F: larger size apo(a) moiety in lipoprotein (a) is associated with higher levels of plasma levels of Lp(a).

A

True

97
Q

Comment about familial hyperlipiadaemia (FH) and Lp(a).

A
  • Lp(a) levels are commonly elevated in FH.

- FH patients with elevated Lp(a) have higher CV risk.

98
Q

What occurs to the following 2 respiratory parameters during the a COPD exacerbation:

  1. End-expiratory lung volume (EELV)
  2. Inspiratory capacity

What is this phenomena called?

A
  1. End-expiratory lung volume (EELV) - increased
  2. Inspiratory capacity - decreased

Dynamic Hyperinflation

99
Q

During dynamic hyperinflation in COPD exacerbation mechanical disadvantages in which 4 respiratory factors occurs?

A
  • Increased PEEPi (intrinsic positive end-expiratory pressure)
  • Decreased dynamic lung compliance
  • Increase elastic threshold loading of inspiratory muscle
  • Inspiratory muscle weakness
100
Q

During dynamic hyperinflation in COPD exacerbation, why is gas exchange impaired?

A

Increased physiological dead space owing to reduced tidal volume.

101
Q

During dynamic hyperinflation in COPD exacerbation leads to neuromechanical uncoupling, how does this manifest symptomatically.

A

Unsatisfied inspiration leading to dyspnoea.

102
Q

During dynamic hyperinflation in COPD exacerbation, what are the 3 cardiovascular effects?

A
  • INCREASED pulmonary arterial pressure
  • DECREASED RV preload
  • INCREASED LV afterload
103
Q

What 8 factors immediately confers high cardiovascular risk status without need for risk calculation.

A

DM (2):

  1. DM and age > 60
  2. DM with microalbuminuria

History (2):

  1. History of CVD (cardiovascular disease)
  2. History of FH
  3. HTN (SBP > 180 or DBP > 110)
  4. Total Cholesterol > 7.5 mmol/L
  5. Aboriginal and age > 74
  6. CKD with eGFR < 45 mL/min/1.73 m^2
104
Q

Patient has a massive pericardial effusion on echocardiogram. What clinical triad do you anticipate?

A
  1. Tachycardia
  2. Low amplitude QRS complex on ECG
  3. Electrical alternans on ECG
105
Q

What is “electrical alternans” on ECG?

What does it suggest?

A
  • consecutive, normally-conducted QRS complexes alternate in height.
  • the heart swings backwards and forwards within a large fluid-filled pericardium.

Massive pericardial effusion

106
Q

HTN is best treated with multiple different antihypertensive agents rather than maximising a single agent. To this end, in which order shoulder the following be commenced in an hypertensive patient with normal renal function:

  1. ACEi / ARB
  2. Thiazide diuretic
  3. Amlodipine
A

ACEi / ARB then Amlodipine then Thiazide diuretic

107
Q

In patient with multi-vessel disease during angiography, non-infarct related arteries with lesions are noted.

Should they be ignored?

A

No - non-culprit lesions need FFR +/- PTCA.

This improves CVS outcomes and reduced revascularisation.

108
Q

What is Dressler’s syndrome?

A

Post-MI immune-mediated

  1. Fever
  2. Pleuritic pain
  3. Pericardial +/- pleural effusion
109
Q

In patients with peripartum CM, familial CM and sporadic idiopathic DCM - which truncating variant is the most prevalent genetic predisposition?

A

TTN - encodes for sarcomere protein titin.

110
Q

Patient has 1st degree relative with HOCM. His history, examination and pertinent investigations reveal no active HOCM. He still needs lifelong screening for HOCM.

How often should this occur in an adult (>18yrs)?

A

Every 5 years

111
Q

Order the following in terms of greatest to least effect on reducing mortality in HFREF:

  1. ACEi
  2. ARB
  3. Spironolactone
  4. BB
A

BB > Spironolactone > ACEi > ARB

112
Q

Use of high dose metoloprolol XR perioperatively reduces cardiovascular event.

Should it therefore be used routinely?

A

No - increased mortality and stroke rates

113
Q

Post-NSTEMI patient with NSTEMI and AF (with CHADVASC > 5) required DAP and anticoagulation for at least 1 month despite bleeding risks and is placed on: aspirin + clopidogrel + warfarin

After 1 month, which agent can be ceased WITHOUT increased rate of thrombotic events.

A

CEASE asprin

Continue clopidogrel + warfarin

114
Q

Patient has resistant HTN already on ACEi, CCB and thiazide.

Which is the best next agent to add to this?

A

Spironolactone

115
Q

Describe the phases of cardiac (ventricular) action potential in terms of (Na/K/Ca/Cl flux)

Phase 0
Phase 1
Phase 2
Phase 3
Phase 4 (Resting)

Remember:
Na / Ca enter cells (in)
K exits cells (out)

A

Phase 0 (steep upslope) - Na in

Phase 1 (pointy bit) - K out

Phase 2 (flat plane) - K out = Ca in

Phase 3 (steep downslope) - K out

Phase 4 (Resting) - K out = Na/Ca in

116
Q

BNP is sometimes used to differentiate HFREF vs. respiratory /other causes of SOB:

  1. Within what range is it not useful?
  2. Above what level is it suggestive of HFREF
  3. Below what level is HFREF unlikely
A
  1. Within what range is it not useful?
    100 - 400 pg/mL = not useful
  2. Above what level is it suggestive HFREF
    >400 pg/mL = HFREF
  3. Below what level is HFREF unlikely
    <100 pg/mL = HFREF unlikely
117
Q

What occurs to BNP in the following scenario:

  1. Obesity
  2. Sepsis / CAD /PAH / valvular disease / increased age / women / renal failure
A
  1. Obesity
    REDUCED
  2. Sepsis / CAD /PAH / valvular disease / increased age / women / renal failure
    INCREASED