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RACP EXAM > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How do you calculate MAP

A

DBP + (1/3 x (SBP-DBP))

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2
Q

What is the normal blood pressure found in the
-Right ventricle
-Pulmonary artery
-Left atrium
-Left ventricle
-Aorta

A

RV: 25/8
PA: 25/8
LA: 8/0
LV: 110/8
Aorta: 110/65

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3
Q

What is FICKS equation

A

VO2 (volume oxygen consumption) = CO x (Arterial- venous oxygen consumption)

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4
Q

What are class I anti-arrhythmic drugs and name some examples

A

Class I anti-arrhythmic drugs= sodium channel blockers
-1a: Procainamide
-1b: Lidocaine
-1c: Flecanide

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5
Q

What are class II anti-arrhythmic drugs

A

B-blockers
Atenolol, Bisoprolol, Propanolol

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6
Q

What affect do Class I anti-arrhythmic drugs have on the ECG

A

Prolong QRS +/- QTc

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7
Q

What are class III anti-arrhythmic drugs and what affect do they have on the ECG

A

Class III- potassium channel blocking
Affect: Prolong re-polarisation - increased QT interval

Examples: Amiodarone

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8
Q

What class of anti-arrhythmic drug is amiodarone

A

Class III- potassium channel blocker

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9
Q

What class of anti-arrhythmic drug is Flecianide

A

Sodium channel blocker

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10
Q

What are class IV anti-arrhythmic drugs. Give an example and explain their effect on the ECG

A

Class IV drugs= calcium channel blockers
Examples: Diltiazem, Verapamil
ECG: slow SA and AV node conduction

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11
Q

Sotolol has properties of 2 classes of anti-arrhythmic drugs- what are they

A

Class II- B blocker + Class III- Potassium channel blocker- at higher doses

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12
Q

Name side effects of Amiodarone

A

Lung- ILD
Liver- hepatotoxicity
Thyroid- hyperthyroid
Skin- photosensitivity

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13
Q

Which valve opens at the end of isovolaemic contraction

A

Aortic valve

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14
Q

At what phase in the cardiac cycle does the aortic valve close

A

Isovolaemic relaxation

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15
Q

Heart sound S1 correlates to which phase of the cardiac cycle

A

Start of isovolaemic contraction

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16
Q

Which phase of the ECG represent isovolaemic contraction

A

QRS complex

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17
Q

Which phase of the ECG represents the ejection phase of the cardiac cycle

A

ST-segment

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18
Q

What causes prolonged splitting of the second heart sound

A

Prolonged RV ejection time e.g RV volume overload (ASD), Pressure overload (e.g. TOF, pulmonary stenosis), RV delayed conduction e.g. RBBB

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19
Q

What is a paradoxical splitting of S2 and what causes it

A

Splitting of the second heart sound during expiration (should split during inspiration)

Causes= LV sustained systole. Can be due to
-increased volume: R–> L shunt, heart failure
-increased ejection pressure: Aortic stenosis
-delayed conduction: LBBB

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20
Q

What do the following aspects of the sinus venous develop into
-common cardinal
-vitilline
-umbilical

A

Common cardinal; you have both a L and R sides. They both have anterior and posterior branches. The posterior branches regress.
-R) anterior cardinal branch- travels upwards to form the R) brachiocephalic vein containing the internal jugular vein and R) subclavian vein.
-L) anterior cardinal branch - travels upwards to form the left brachiocephalic vein.
-L) and R) brachiocephalic veins then fuse to form a shunt known as the SVC
-On the left side, any aspect of the left cardinal vein beneath this shunt is supposed to regress .

Vitilline duct: Travel to the yolk sac and form a GI venous plexus and hepatic plexus. Fuse to form the IVC

Umbilical: forms the ductus venous and drains into the IVC

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21
Q

What is formed by the following aortic arches
1-
2-
3-
4-
5-
6-

A

1- MAX (i.e. first is the MAX you can be)- Maxillary artery
2- “Second” = Stapedial artery
3- “C is the first letter in alphabet”- Carotids - becomes right and left common carotids
4- “4 limbs”- right and left subclavian arteries + aortic arch (which becomes descending aorta to supply blood to the feet)
5- degenerates
6- 96 = 2 lung= pulmonary arteries + ductus arteriosus

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21
Q

What is formed by the following aortic arches
1-
2-
3-
4-
5-
6-

A

1- MAX (i.e. first is the MAX you can be)- Maxillary artery
2- “Second” = Stapedial artery
3- “C is the first letter in alphabet”- Carotids - becomes right and left common carotids
4- “4 limbs”- right and left subclavian arteries + aortic arch (which becomes descending aorta to supply blood to the feet)
5- degenerates
6- 96 = 2 lung= pulmonary arteries + ductus arteriosus

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22
Q

How does the primitive pulmonary veins form

A

-Lung bud is formed from foregut
-Creates a splanchnic plexus which initially is connected to umbilical and vitilline venous system
-At day 28, left atrium forms a primordial invagination - common pulmonary vein
-Splanchnic plexus also differentiates into pulmonary vascular bed and grows down to connect to the new pulmonary vein
-Once connection is made, the cardinal and umbilicovitilline connection degenerates

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23
Q

What occurs to cause total anomalous pulmonary venous connection

A

-At day 28, left atrium forms a primordial invagination - common pulmonary vein
-Splanchnic plexus in the primitive lung also differentiates into pulmonary vascular bed and grows down to connect to the new pulmonary vein
-Once connection is made, the cardinal and umbilicovitilline connection is supposed to degenerate

-Failure to do so= TAPV
-If cardinal system is retained: connection of lung to the SVC, RA
-If umbilicovitilline system retain: connection to the IVC, hepatic or portal system

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24
Q

What SpO2 would there be before you detected clinical cyanosis in the below patients
-normal Hb
-anaemia
-polycythamia

A

-normal: 80%
-anaemia: 50%
-polycythaemia: 84%

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25
Q

What affect do the following conditions have on the oxygen-hb desaturation curve
-acidosis
-increased diphosphoglycerate
-increased fetal Hb
-Carbon monoxide
-Hypothermia

A

-Low pH shifts the curve to the Right, reducing affinity to Hb
-DPG made by cells in glycolysis during hypoxia. Increased level = increased hypoxia = shifts curve right

-fetal Hb= increased affinity for oxygen= shifts curve left
-CO= increased affinity for oxygen= shifts curve left
-Low temp= shifts curve left= increased affinity for oxygen

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26
Q

What murmur do you get with a
-secundum ASD
-primum ASD

A

-ASD= pulmonary flow murmur + fixed splitting of the second heart sound
-Primum = ASD close to the endocardial cushion which can affect the AV valves and result in MR. Murmur will be a pan systolic + pulmonary flow + fixed splitting of S2

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27
Q

What CHD is most associated with trisomy 21

A

AVSD

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28
Q

Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects

A

COX 1+ 2 inhibitor - reduced circulating prostaglandins

SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH

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28
Q

Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects

A

COX 1+ 2 inhibitor - reduced circulating prostaglandins

SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH

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29
Q

What is the Rastelli procedure and for what congenital heart defect is it performed

A

Performed for Truncus arteriosus
Involves sealing the VSD so that the LV pumps into the Truncus and then making a homograft connection from the RV to the main posterior pulmonary artery

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29
Q

What is the Rastelli procedure and for what congenital heart defect is it performed

A

Performed for Truncus arteriosus
Involves sealing the VSD so that the LV pumps into the Truncus and then making a homograft connection from the RV to the main posterior pulmonary artery

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30
Q

What is the difference between L-TGA and D-TGA

A

D-TGA: have parallel circuits. Right and left ventricles + atrium are normally positioned however aorta is connected to RV and pulmonary trunk to the left ventricle.
Need a PDA and ASD/VSD for mixing to survive

L-TGA: congenitally corrected TGA. Inlet and outlet vasculature is “normally” connected however LV and RV sites are switched

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31
Q

What is the classical CXR finding for Transposition of the great arteries

A

Egg on a string

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32
Q

Describe the Senning Procedure and when it is used

A

Used to correct Loop-TGA (where the ventricles are on opposite sides but the rest of the atrial and arterial aspects are normally placed

-PA band to build up strength of left ventricle which up to that point has been pumping to the pulmonary trunk
-Intra-atrial baffle placed to redirect systemic blood from the IVC+SVC –> Right atrium and visa versa for the pulmonary blood –> LA
-Arterial switch operation where great arteries transected and placed in correct anatomical positions

33
Q

Describe the 3-step palliative cardiac pathway involved with a single ventricle e.g. severe tricuspid atresia

A

1) Blolock-Thaussig shunt- 1st week of life- shunt from subclavian to pulmonary artery to increased pulmonary blood flow

2) Bidirectional Glenn- SVC anastomosis to the pulmonary artery
3) Fontan- IVC anastomosed to the pulmonary artery

At end of Fontan have 2 separate circulations and single ventricle system where systemic blood bypasses the heart

34
Q

What on a ECG would differentiate a VSD from tetralogy of fallot

A

VSD: get LVH
TOF: get RAD and RVH

35
Q

Describe the 3 steps used in the palliative correction of HLHS

A

1) Norwood: aim to reconstruct the aorta and improve systemic circulation.
-ASD created
-Pulmonary trunk cut. Distal end is closed so the heart no longer directly supplies the pulmonary arteries
-Proximal end connected to native aorta with homograft material used to reconstruct its size
-BT shunt created to shunt blood from R) subclavian artery to the R) pulmonary artery.
-Sanno shunt may be created to direct some blood from the RV to the pulmonary arteries

2) Bidirectional Glenn- SVC cut and connected to the R) pulmonary artery
3) Fontann- IVC cut and connected directly to the R) pulmonary artery

END circulation: IVC + SVC directed via shunt to the pulmonary artery –> lungs –> pulmonary veins –> LA – (ASD) –> RA –> RV –> Neo-aorta –> circulation

36
Q

What valvular lesion is Williams syndrome associated with

A

Supra valvular stenosis- aortic and pulmonary

37
Q

What valvular lesion is Alagiles associated with

A

Peripheral pulmonary artery stenosis

38
Q

What value issue is Turners associated with

A

Coarctation of the aorta + bicuspid aortic valve

39
Q

What valve issues is Noonans associated with

A

Valvular pulmonary stenosis

40
Q

How might an older child with Coarctation of the aorta present

A

Leg pain after exercise
Reduced ETT
Hypertension

On exam- ESM, LVH
CXR- 3 sign, rib notching
ECG: LAD, LVH

41
Q

What murmur does mitral stenosis give you

A

Mid diastolic rumble

42
Q

what murmur is associated with marfans syndrome

A

Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation

42
Q

what murmur is associated with marfans syndrome

A

Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation

43
Q

Name 3 clinical signs of aortic regurgitation

A

-decrescendo diastolic murmur
-wide pulse pressure
-collapsing pulse
-signs of left heart failure

43
Q

Name 3 clinical signs of aortic regurgitation

A

-decrescendo diastolic murmur
-wide pulse pressure
-collapsing pulse
-signs of left heart failure

44
Q

What is the risk to the next child is a
-parent
-sibling
is affected by congenital heart disease

A

Parent- 4-5%
Sibling 2-4%
Usual: 0.8%

45
Q

What is patau syndrome, its features and what CHD is it associated with

A

Patau = trisomy 13
Sx; midline effects e.g. cleft lip and palate, microcephaly, coloboma, polydactyl, Holoprosencephaly

CHD: 80% have it- ASD, VSD- most common. Also seen with HLHS

46
Q

What is Edwards syndrome
What are its clinical features
What CHD is it associated with

A

Edwards= trisomy 18
Clinical features: rocker bottom feet, hypertonia, arthrogryposis, omphalmocoele, reduced IQ

90-100% have CHD- ASD/VSD most common
Also get PDA, CoA, TOF, DORV

47
Q

What are the symptoms of DiGeorge syndrome including what CHD is associated with it and was is the genetic abnormality

A

“CATCH-22”
-Cardiac abnormaliteis- conotruncal defects
-Abnormal facies: low set ears, long nose, short philtrium, micrognathia
-Thymic aplasia
-Cleft palate/ bifid uvula
-Hypocalcamia/ hypoparathyrodis,
-22q11 micro deletion

48
Q

What is the most common CHD associated with 22q11 micro deletion

A

Tetralogy of Fallot- 35%

Followed by- interrupted aortic arch (20%) and Truncus arterioles (10%)

49
Q

A child presents with hypertension and a ejection systolic murmur plus dysmorphic facial features- what is the likely syndrome

What electrolyte abnormality are they most likely to get

A

Williams
-supravalvular aortic or pulmonary stenosis
-renal artery stenosis causes hypertension
-facial feature: elfin like facies, long philtrum, broad forehead, short nose

-Hypercalcaemia

50
Q

A child presents with jaundice, a triangular face and a systolic murmur. What is the likely diagnosis and CHD

A

Allagiles- peripheral pulmonary stenosis

51
Q

What is the mutation in Marfans syndrome and what CHD does it cause

A

FBN1 mutation- for fibrillin
Aortic root dilatation

52
Q

Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD

A

AD - mutation in the RAs/mitogen activated protein signalling pathway
CHD- valvular pulmonary stenosis
(+HOCM)

52
Q

Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD

A

AD - mutation in the RAs/mitogen activated protein signalling pathway
CHD- valvular pulmonary stenosis
(+HOCM)

53
Q

What are the criteria for infective endocarditis called and what are they

A

Dukes Criteria
-2 major OR 1 major 3 minor OR 5 minor

Major
-Microbiological evidence of IE
*1x PBC +ve for Coxiella
*2xPBC +ve for typical agent
*3x PBC +ve for atypical agent

-Echocardiogram evidence: new vegetation, lesion, regurgitation, abscesses, or dehisistance of a mechanical valve

Minor criteria
-Risk factors for IE: CHD, previous IE, RHD, CVC, Prosthetic valve, mitral valve prolapse
-Fever >38
-Immunological evidence: Oslers nodes, nephritis (haematuria/proteinuria), Rheumatoid factor +Ve, low complement
-Vascular phenomena: splinter haemorrhages, Janeway lesions, Roths spots
-+ve blood culture not meeting major criteria

54
Q

Who receives IE prophylaxis before a dental procedure

A

-Previous IE, RHD, prosthetic valve
-CHD with stents or unrepaired/palliation
-CHD with repair <6 months ago

55
Q

What are the criteria for diagnosis of rheumatic fever

A

JONES criteria
-2 major OR 1 major 2 minor = definitive
-1 major, 1 minor, preceding GAS = probable

Evidence of preceding GAS (ASOT and Anti-DNAse titres or throat swab)
PLUS
Major- JONES
-Joints- polyarthritis
-O-Carditis- new MR, AR, pericarditis, myocarditis, subclinical endocarditis on echocardiogram
-Nodules- subcutaneous nodules
-Erythema margiatum
-Sydenem chorea- can be used to diagnosis RF in isolation

Minor criteria
-Arthralgia
-Fever >38
-Elevated ESR and CRP
-Prolonged PR interval

56
Q

How long do you give IM Benpen in RHD for
-minor MR
-moderate MR
-severe MR

A

minor: 10 years or until 21y/old which ever is longer
moderate: age 35
severe: age 40

57
Q

Name features of Kawasaki disease
What investigations would you do

A

Fever > 5 days
Cervical lymphadenoapthy
Mucositis
Macular rash
Red hands/feet +/- desquamation
Non exudative conjunctivitis

Investigations:
-Increased ESR/CRP
-FBC: low/high WCC, thrombocytosis
-Electrolytes: low sodium and albumin
-LFTs; Increased
-Urine: sterile puria
-Echo: effusion, aneurysm, myocardial dysfunction, valvular issues

58
Q

What medication is contraindicated in HOCM

A

Digoxin- increases contractility of the heart which can worsen the LVOTO

59
Q

What glycogen storage disorder causes HOCM

A

Pompe disease

60
Q

What dose of aspirin and IVIG do you give in Kawasaki Disease

A

IVIG- 2mg/kg
Aspirin- 7-12.5mg/kg QID until fever resolves
Then low dose (3-5mg/kg daily) for min 6/52

61
Q

What genetic defect causes genetic HOCM

A

Autosomal dominant defect in cardiac B myosin

62
Q

Describe aortic dissection types I, II and III
What conditions might they be seen in

A

Type I; ascending aorta and extending distally
Type II: ascending aorta and limited to the arch
Type III: beginning after L) subclavian artery

Ehlos Danlos + Marfan syndrome

63
Q

Name the Mechanism of action of Digoxin
When is it contra-indicated

A

Inhibits membrane Na/K ATPas. Reverses the Na/Ca exchanger which would normally pump calcium out of the cell and sodium into the cell. Result = increased intra-cellular calcium to improve cardiac contractility.

Also releases myocardial norepinephrine –> affects the B1 receptors

C/I in HOCM + LVOTO

64
Q

Name the MoA of action Dopamine and Dobutamine

A

dopamine: increases myocardial norepinephrine
dobutamine: B1 receptor agent

Dobutamine: synthetic catecholamine which acts as beta agonist –> positive inotropic and chronotrophic effect

65
Q

What is the MoA of Enalapril and Captopril

A

ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone –> reduce blood volume

Reduced angiotensin II also results in vasodilation therefore reduced PVR

65
Q

What is the MoA of Enalapril and Captopril

A

ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone –> reduce blood volume

Reduced angiotensin II also results in vasodilation therefore reduced PVR

66
Q

What is the MOA of Frusemide
What electrolyte abnormality can it cause

A

Blocks Na/2Cl/K reabsorption in the Loop of Henle and distal tubule

Hypokalaemia

67
Q

What is the MoA of Spironolactone

What is its advantage compared to other diuretics

A

Blocks Aldosterone - aldosterone agonist

Potassium sparing

68
Q

What is the MoA of Chlorthiazide

A

Blocks Na/Cl resorption
in the distal convoluted tubule

69
Q

Why are ACE inhibitors Contraindicated in LVOTO

A

Concerns about poor coronary artery perfusion if after load is reduced and diastolic coronary artery perfusion is impaired

70
Q

What is the MoA of Milrinone

A

Phosphodiesterase inhibitor - prevents degradation of cAMP –> positive inotropy

note: cAMP= increased opening of L-calcium channels

70
Q

What is the MoA of Milrinone

A

Phosphodiesterase inhibitor - prevents degradation of cAMP –> positive inotropy

note: cAMP= increased opening of L-calcium channels

71
Q

What changes are seen in the ECG with hypokalaemia

A

Flattened T-waves with some inversion
U-waves
“long QT” due to fused T+U waves

72
Q

What changes are seen in hyperkalaemia

A

Tall peaked T-waves
Shortened QT interval- faster repolarisation
Prolonged PR and QRS interval

73
Q

What does hypocalcaemia do to the ECG and why

A

Prolongs the QT interval

L) voltage calcium channels only inactivated once intra-cellular calcium reaches a certain threshold. If low calcium levels, takes longer to do so = prolonged plateau phase of cardiac cycle = prolonged QTc

74
Q

Describe the difference between Mobiz type I and II heart block

A

Mobiz I: progressive lengthening of PR interval until there is a drop of the p wave
Mobiz II: sudden non-conduction of a p-wave. Due to fibrosis at the AV node. At risk of progressing to type III block

74
Q

Describe the difference between Mobiz type I and II heart block

A

Mobiz I: progressive lengthening of PR interval until there is a drop of the p wave
Mobiz II: sudden non-conduction of a p-wave. Due to fibrosis at the AV node. At risk of progressing to type III block

75
Q

What is the key feature you see with focal atrial tachycardia on ECG and what is first line treatment

A

p-waves of variable morphology but still in sinus rhythm

B-blockers
May need Radiofrequency ablation

76
Q

What do you see on ECG in atrial flutter
What causes it
What is the treatment

A

Sawtooth pattern
Re-entrant circuit contained to the atria. AV node prevents conduction this, resulting in a 2:1 or 3:1 block

TX= synchronised DC cardio version 0.5-2J/kg
May need Amiodarone + B-blocker

RACP EXAM (9 decks)

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