Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

RACP EXAM > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How do you calculate MAP

A

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

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

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

What is FICKS equation

A

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

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

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

What are class II anti-arrhythmic drugs

A

B-blockers
Atenolol, Bisoprolol, Propanolol

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

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

A

Prolong QRS +/- QTc

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

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

What class of anti-arrhythmic drug is amiodarone

A

Class III- potassium channel blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What class of anti-arrhythmic drug is Flecianide

A

Sodium channel blocker

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

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

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

Name side effects of Amiodarone

A

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

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

Which valve opens at the end of isovolaemic contraction

A

Aortic valve

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

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

A

Isovolaemic relaxation

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

Heart sound S1 correlates to which phase of the cardiac cycle

A

Start of isovolaemic contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which phase of the ECG represent isovolaemic contraction

A

QRS complex

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

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

A

ST-segment

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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
What SpO2 would there be before you detected clinical cyanosis in the below patients -normal Hb -anaemia -polycythamia
-normal: 80% -anaemia: 50% -polycythaemia: 84%
25
What affect do the following conditions have on the oxygen-hb desaturation curve -acidosis -increased diphosphoglycerate -increased fetal Hb -Carbon monoxide -Hypothermia
-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
26
What murmur do you get with a -secundum ASD -primum ASD
-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
27
What CHD is most associated with trisomy 21
AVSD
28
Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects
COX 1+ 2 inhibitor - reduced circulating prostaglandins SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH
28
Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects
COX 1+ 2 inhibitor - reduced circulating prostaglandins SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH
29
What is the Rastelli procedure and for what congenital heart defect is it performed
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
29
What is the Rastelli procedure and for what congenital heart defect is it performed
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
30
What is the difference between L-TGA and D-TGA
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
31
What is the classical CXR finding for Transposition of the great arteries
Egg on a string
32
Describe the Senning Procedure and when it is used
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
Describe the 3-step palliative cardiac pathway involved with a single ventricle e.g. severe tricuspid atresia
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
What on a ECG would differentiate a VSD from tetralogy of fallot
VSD: get LVH TOF: get RAD and RVH
35
Describe the 3 steps used in the palliative correction of HLHS
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
What valvular lesion is Williams syndrome associated with
Supra valvular stenosis- aortic and pulmonary
37
What valvular lesion is Alagiles associated with
Peripheral pulmonary artery stenosis
38
What value issue is Turners associated with
Coarctation of the aorta + bicuspid aortic valve
39
What valve issues is Noonans associated with
Valvular pulmonary stenosis
40
How might an older child with Coarctation of the aorta present
Leg pain after exercise Reduced ETT Hypertension On exam- ESM, LVH CXR- 3 sign, rib notching ECG: LAD, LVH
41
What murmur does mitral stenosis give you
Mid diastolic rumble
42
what murmur is associated with marfans syndrome
Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation
42
what murmur is associated with marfans syndrome
Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation
43
Name 3 clinical signs of aortic regurgitation
-decrescendo diastolic murmur -wide pulse pressure -collapsing pulse -signs of left heart failure
43
Name 3 clinical signs of aortic regurgitation
-decrescendo diastolic murmur -wide pulse pressure -collapsing pulse -signs of left heart failure
44
What is the risk to the next child is a -parent -sibling is affected by congenital heart disease
Parent- 4-5% Sibling 2-4% Usual: 0.8%
45
What is patau syndrome, its features and what CHD is it associated with
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
What is Edwards syndrome What are its clinical features What CHD is it associated with
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
What are the symptoms of DiGeorge syndrome including what CHD is associated with it and was is the genetic abnormality
"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
What is the most common CHD associated with 22q11 micro deletion
Tetralogy of Fallot- 35% Followed by- interrupted aortic arch (20%) and Truncus arterioles (10%)
49
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
Williams -supravalvular aortic or pulmonary stenosis -renal artery stenosis causes hypertension -facial feature: elfin like facies, long philtrum, broad forehead, short nose -Hypercalcaemia
50
A child presents with jaundice, a triangular face and a systolic murmur. What is the likely diagnosis and CHD
Allagiles- peripheral pulmonary stenosis
51
What is the mutation in Marfans syndrome and what CHD does it cause
FBN1 mutation- for fibrillin Aortic root dilatation
52
Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD
AD - mutation in the RAs/mitogen activated protein signalling pathway CHD- valvular pulmonary stenosis (+HOCM)
52
Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD
AD - mutation in the RAs/mitogen activated protein signalling pathway CHD- valvular pulmonary stenosis (+HOCM)
53
What are the criteria for infective endocarditis called and what are they
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
Who receives IE prophylaxis before a dental procedure
-Previous IE, RHD, prosthetic valve -CHD with stents or unrepaired/palliation -CHD with repair <6 months ago
55
What are the criteria for diagnosis of rheumatic fever
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
How long do you give IM Benpen in RHD for -minor MR -moderate MR -severe MR
minor: 10 years or until 21y/old which ever is longer moderate: age 35 severe: age 40
57
Name features of Kawasaki disease What investigations would you do
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
What medication is contraindicated in HOCM
Digoxin- increases contractility of the heart which can worsen the LVOTO
59
What glycogen storage disorder causes HOCM
Pompe disease
60
What dose of aspirin and IVIG do you give in Kawasaki Disease
IVIG- 2mg/kg Aspirin- 7-12.5mg/kg QID until fever resolves Then low dose (3-5mg/kg daily) for min 6/52
61
What genetic defect causes genetic HOCM
Autosomal dominant defect in cardiac B myosin
62
Describe aortic dissection types I, II and III What conditions might they be seen in
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
Name the Mechanism of action of Digoxin When is it contra-indicated
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
Name the MoA of action Dopamine and Dobutamine
dopamine: increases myocardial norepinephrine dobutamine: B1 receptor agent Dobutamine: synthetic catecholamine which acts as beta agonist --> positive inotropic and chronotrophic effect
65
What is the MoA of Enalapril and Captopril
ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone --> reduce blood volume Reduced angiotensin II also results in vasodilation therefore reduced PVR
65
What is the MoA of Enalapril and Captopril
ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone --> reduce blood volume Reduced angiotensin II also results in vasodilation therefore reduced PVR
66
What is the MOA of Frusemide What electrolyte abnormality can it cause
Blocks Na/2Cl/K reabsorption in the Loop of Henle and distal tubule Hypokalaemia
67
What is the MoA of Spironolactone What is its advantage compared to other diuretics
Blocks Aldosterone - aldosterone agonist Potassium sparing
68
What is the MoA of Chlorthiazide
Blocks Na/Cl resorption in the distal convoluted tubule
69
Why are ACE inhibitors Contraindicated in LVOTO
Concerns about poor coronary artery perfusion if after load is reduced and diastolic coronary artery perfusion is impaired
70
What is the MoA of Milrinone
Phosphodiesterase inhibitor - prevents degradation of cAMP --> positive inotropy note: cAMP= increased opening of L-calcium channels
70
What is the MoA of Milrinone
Phosphodiesterase inhibitor - prevents degradation of cAMP --> positive inotropy note: cAMP= increased opening of L-calcium channels
71
What changes are seen in the ECG with hypokalaemia
Flattened T-waves with some inversion U-waves "long QT" due to fused T+U waves
72
What changes are seen in hyperkalaemia
Tall peaked T-waves Shortened QT interval- faster repolarisation Prolonged PR and QRS interval
73
What does hypocalcaemia do to the ECG and why
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
Describe the difference between Mobiz type I and II heart block
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
Describe the difference between Mobiz type I and II heart block
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
What is the key feature you see with focal atrial tachycardia on ECG and what is first line treatment
p-waves of variable morphology but still in sinus rhythm B-blockers May need Radiofrequency ablation
76
What do you see on ECG in atrial flutter What causes it What is the treatment
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions