Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FRACP 2023 Cram Homicrons Edition > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Most common cause of dilated cardiomyopathy

A

50% Idiopathic
46% myocarditis (adeno, entero, HHV6/coxsackie, CMV)
35% genetic (mainly neuromuscular disease)

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

Most common cause of HOCM

A

30-60% inherited- AD mutations in sarcomeric proteins
- Troponin T mutations: beta-myosin heavy chain MYH7 and myosin binding protein C MYBPC3
- 50% spontaneous

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

HOCM associated syndromes

A

Noonan, BWS, LEOPARD, Friedrich Ataxia

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

Echo findings in obstructive HOCM

A

HOCM - systolic anterior motion (SAM) of the mitral valve against the hypertrophied septum

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

Treatment of HOCM

A

Exercise restriction, B-blockers, myotomy, antiarryhmics, ICD if high risk

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

Features of restrictive cardiomyopathy, prognosis?

A

Diastolic dysfunction with normal LV thickness
- Biatrial enlargement on Echo
- Poor prognosis, progressively worsens
- Rare 5% of childhood CM
- DDx constrictive pericarditis

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

Features of arrythmogenic RV cardiomyopathy

A

RV myocardium replaced by fatty/fibrous tissue, systolic bulging of RV wall

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

Pathophys of CCF- compensatory mechanisms heart/kidney

A

Decreased SV + CO
- Ventricular dilatation/hypertrophy
- Increased EDP/impaired filling (eventually SV cannot increase and plateaus)
- Increased SNS activation- HR & contractility ^ - damages myocardium chronically
- Dec RBF = inc RAAS (Ang 2 = inc Na/H20 reabs/vasoconstriction- promotes myocardial fibrosis)

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

DDx 12wk baby presenting with failure

A

VSD, ALCAPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rejection prevention in heart transplant?

A

Triple therapy: CNI (tacro/evero/sirolimus) + cyclosporin/antimetabolite/WBC enzyme inhibitor (AZA/MMF/6MP) + prednisolone

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

Most common cause of post transplant infection

A

CMV 25%
- consider IV gancyclovir prophylaxis if donor CMV +ve

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

Difference in pathophys acute cellular vs humoral vs chronic transplant rejection

A
  • Acute cellular: T cell mediated, may have antibodies (ATGAM, OKT3)
  • Acute humoral: alloantibodies to HLA/endothelial antigens (complement staining on Bx)
  • Chronic: diffuse immune mediated, cause unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PHTN: common vasodilators

A
  1. NO (endothelial release) - increases cGMP, diffuses into smooth musc to vasodilate, PDE breaksdown, PDE inhibitors (i.e sildenafil) ^ vasodilation
  2. Arachadonic acid pathway- prostaglandin I2/prostacyclin
  3. Adenosine
  4. Oxygen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PHTN: vasoconstrictors

A
  1. Hypoxia potent vasoconstrictor (pulm oedema, PE, lung compression)
  2. ET-1
  3. Thromboxane A2
  4. Vasoconstriction from SNS overactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Features of Eisenmengers

A

Shunt reversal R-L in acyanotic lesion - VSD classical, also ASD, AVSD/ECD, PDA
- Influenced by pulm pressure, PBF & hypoxia
- Grade 1-5 based on severity of small arteriolar obstruction
- Usually 2nd/3rd decade, T21 earlier
- Resistant to medical Mx

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

Risk factors/causes of PPHN

A

MAS 41%, pneumonia/RDS 15%, CDH 10%, pulm hypoplasia 5%, idiopathic 20%

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

Causes of PPHN

A
  1. Vasoconstriction with normal vasculature
    - Alveolar hypoxia- MAS, HMD, CNS hypoventilation
    - Birth asphyxia, shock
    - Infections
    - Polycythemia
  2. Arteriolar hypertrophy
    -Intrauterine asphyxia
    - Maternal meds
  3. Developmentally abnormal vasculature
    - CDH, pulm hypoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Most common infective endocarditis organisms

A

Prev >90% strep viridians, staph aureus & enterococci

Rise of HACEK
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikinella
- Kingella

S.Viridians most common after dental surgery
Staph most common post op
Enterococcus most common post GI/GU surgery

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

Indications for IE prophylaxis

A
  • Prev IE
  • Prosthetic heart valves
  • Unrepaired cyanotic CHD, CHD with prosthetic device/residual defect
  • Heart transplant patients
  • ?ASD/repaired ASD/PDA

Pre-op (dental, mouth/skin/MSK)
high risk- as above
Not indicated in low risk- acquired valve disease, pacemakers, repaired acyanotic CHD

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

Indications for IE prophylaxis

A
  • Prev IE
  • Prosthetic heart valves
  • Unrepaired cyanotic CHD, CHD with prosthetic device/residual defect
  • Heart transplant patients

Pre-op (dental, mouth/skin/MSK)
high risk- as above
Not indicated in low risk- ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most common cause of myocarditis, mortality risk assoc.

A

Viral- adeno, entero, echino
Up to 75% mortality

Rx bed rest, high dose IVIG, CCF meds (diuretics, inotropes), ACEi/antiarrythmics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most common cause of myocarditis, mortality risk assoc.

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

Most common cause of pericarditis by age group

A

Infant/young children: viral
Older children: ARF, bacterial (S.Aureus, H.Influenza, N.Meningitidis)

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

Mx of constrictive pericarditis and outcomes

A

Pericardial resection - improvement in 75% of patients

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

Features of KD

A

Fever >5days + 4/5 of
- Conjunctivitis: bilateral/non purulent
- Lymphadenopathy: unilateral/tender
- Rash: polymorphous
- Mucosal changes: oral hyperemia, strawberry tongue
- Extremity changes: hyperemia -> desquamation

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

Features of incomplete KD

A

Fever >5d + 2-3 of:
- irritability without explaination
- unexplained aseptic meningitis
- shock
- cervical adenitis not responsive to ABx

Lab findings suggestive
- anaemia
- raised plts >450, WCC >15, urine WBC >10
- low albumin <30
- abnormal echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Incidence of coronary artery aneurysm
(incidence if treated with IVIG)

A

15-25%
With IVIG 4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

High risk for CAA with KD

A

Signs of shock
Age <12 months
Asian ethnicity
ALT > 100
Alb < 30
Evidence of cardiac involvement at presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Timing of echo for CAA monitoring in KD

A

At presentation (this should not delay initiation of treatment)
2 weeks
6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Major criteria for ARF

A

ACHES
Arthritis
Chorea
Heart-carditis
Erythema marginatum
Subcut nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Minor criteria for ARF

A

TAPE
Temp >38
Arthralgia
PR prolongation
Elevated CRP/ESR >30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Most common presenting feature of ARF?

A

Arthritis

Nb: Chorea rare, but up to 25% in ATSI adolescent females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Duration of benzathine penicillin (IM 4/52) prophylaxis in ARF?

A

10yrs since last episode ARF or 21yrs of age, whichever longer…. OWCH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Management of VT?

A

Pulse present- amiodarone 5mg/kg/30mins
No pulse- Synchronous DC shock 2J/kg > 4J/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of VF

A

Shockable rhythm
- 4J/kg synchronous shock
- CPR 2mins- pulse check
- Adrenaline 10mcg/kg after 2nd shock then every 2nd loop CPR
- Amiodarone 5mg/kg after 3rd shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Management of SVT

A

Vagal stimulation- ice/vasovagal
If haemodynamically stable: Adenosine - 100, 200, 300mcg/kg
If shocked: synchronous DC shock 1J > 2J/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Most common cause of congenital complete heart block

A

Neonatal lupus 60-90% (autoimmune Abs cross placenta)
Congenital heart disease 25-33%- L-TGA, single ventricle pathologies, polysplenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Causes of long QT

A

A: Anti Arrhythmics – amiodarone, sotalol, quinidine
B: Anti Biotics – macrolides, bactrim, erythromycin
C: Anti- psyChotics – haloperidone, risperidone, chlorpromazine
D: Anti – Depressants – tricyclics
E: Low Electrolyes/ Endocrine: low Ca, low K, low Mg, hypothyroidism
F: Anti-Fungals: fluconazole
G: Bad Genes
H: Anti Histamines – terfinadine, astemizole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Genetic/Syndromic long QT

A

K+ - 30% KCNQ1/ 30% KCNH2 - triggered by emotion/exercise
Na2+ channel- 10% SCN5A

Syndromes:
Roman Ward (AD)- most common, multiple genes- LQTS 1-3,5,6,9-15
Jervell-Lange-Neilsen (AR) KCNQ1/NE1- SNHL
Anderson-Tarwil (AD) KCNJ2- muscle weakness/dev delay
Timothy (AD)- L Type Ca2+ channel (CACNAIC)- webbed digits, developmental delay, hypoglycemia, immunodeficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Symptoms/presentation of LQTS

A

Asymptomatic/positive FHx 60%
Symptoms = syncope (26%), seizure (10%), cardiac arrest (9%), pre-syncope, palpitations (6%), deafness (5%)

Triggers:
LQT1 – attacks during exercise/ swimming, broad based T waves
LQT2 – response to sudden noise, low amplitude T waves
LQT3 – attacks during rest/ sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Indications for VSD repair

A
  • Qp:Qs >2:1
  • CCF not responding to MMx
  • Symptoms despite max therapy
  • T21 (early repair)

Contraindications:
- PVR >12 WU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Ficks formula

A

Qp:Qs = (SaO2 - MvO2) / (PvO2 - PaO2)

SaO2 = Aortic SpO2
MvO2 = mixed venous SpO2 (SVC or RA)

PvO2 = Pulmonary vein SpO2
PaO2 = Pulmonary artery oxygen SpO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Murmur, ECG & CXR findings: VSD

A

Pansystolic- LLSB
ECG: LVH/BVH if severe
CXR: Increased PA markings, LA/LVH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Murmur, ECG & CXR findings: AVSD

A

Murmur: pansystolic/holosystolic LLSB (MR) + diastolic rumble, narrow split S2
CXR: cardiomegaly, increased PA markings
ECG: BVH/superior axis, prolonged PR

43
Q

Murmur, ECG & CXR findings: ASD

A

Murmur: Ejection systolic murmur LUSB + click, widely split fixed S2 (prolonged closure of the pulmonary valve)
CXR: Increased PA markings
ECG: RVH + RBBB

44
Q

Murmur, ECG & CXR findings: PDA

A

Murmur: machinery murmur/continuous LUSB
ECG: BVH
CXR: L) enlargement

45
Q

Murmur, ECG & CXR findings: PAPVR

A

Murmur: Ejection systolic murmur LUSB- +/- click, fixed S2 if assoc with ASD
ECG: RVH
CXR: R) enlargement, increased PA markings, scimitar sign

46
Q

Murmur, ECG & CXR findings: TAPVR

A

Murmur: Ejection systolic murmur LUSB + diastolic rumble LLSB, split + fixed S2
ECG: RAH/VH & RAD
CXR: R) enlargement, snowman sign

47
Q

Murmur, ECG & CXR findings: AS

A

Murmur: Systolic murmur-ESM RUSB, Early crescendo LLSB if bicuspid + paradoxical split S2 (expiration) if severe
ECG: LVH/N
CXR: N/dilated AO

48
Q

Murmur, ECG & CXR findings: PS

A

Murmur: Ejection systolic LUSB- radiates to back, wide split A2/P2 (prolonged closure of the pulmonary valve.)
ECG: RAD/RVH
CXR: Enlarged main PA/ cardiomegaly & increased PA markings if severe

49
Q

Murmur, ECG & CXR findings: coarctation

A

Murmur: Ejection systolic- RUSB/LLSB- paravertebral interscapular ares (heard best posteriorly)
- single loud S2
ECG: RVH/RBBB- LVH if severe/asymptomatic
CXR:Cardiomegaly/pulm oedema if symptomatic, rib notching if asymptomatic

50
Q

Murmur in ASD + cause?

A

Systolic, loudest in LUSE (flow across PV), widely split S2- due to RBBB +/- diastolic murmur in large ASD (flow across TV)

51
Q

Features of complete AVSD & Mx

A

Primum + inlet VSD + abnormal MV/TV
- Early CCF 1-2mo post birth, PVOD 6-12mo, DEATH 2-3yrs
- Holosystolic murmur, diastolic murmur + narrow split S2/loud S1
- Superior axis ECG
- BVH, ^ pBF & PA on XR
- Rx surgery 2-4mo,
T21 at worse risk

52
Q

Timing of surgical Mx for VSD, ASD & indications

A

ASD: >8mm unlikely to close (3mm 100%, 3-8mm >80%), device closure at 2-4yrs - if Qp:Qs >5:1,RV overload/CHF

VSD: inlet/outlet do not close- device close 6-12mo- if Qp:Qs >2:1, CHF, PVOD

53
Q

Timing of VSD closure

A

60% small muscular VSD close (<8y)
30% small perimembranous VSD close (<5y)
Inlet + outlet do NOT close

54
Q

Mx severe ASD

A

PGE infusion

Balloon valvuloplasty
- Indications: duct dependent, ↓ LV function, gradient >50 mmHg

Surgical
- Norwood procedure + Fontan if critical AS with hypoplastic L) heart
- Ross procedure: AV replaced with PV
- Artificial valve

55
Q

most common cause aortic stenosis /associations?

A

Valvular (75% BV)
– Turner (bicuspid AV)

Supra-valvular
- William
- Familial hyper-chol

56
Q

Findings in co-arctation

A

Symptomatic - stenosis/reduced BF past aorta, RVH
Asymptomatic- collaterals develop

UL>LL BP 15-20mmHg
Reduced/absent femorals
ESM- RUSB & LLSB- continuous murmur if collaterals
Rib notching on CXR if collaterals
ECG: LAD/LVH - asymptomatic RAD/RVH/RBBB if symptomatic

57
Q

Syndromes associated with MVP

A

Marfan
EDS
OI
Stickler
PCKD (adults)
Klinefelter

58
Q

Conditions associated with MR

A

Rheumatic fever, KD
MPS- Hurler syndrome

59
Q

Syndromes associated with AR

A

Marfan, Ehler-Danlos, MPS- Hurler Sx

60
Q

Cyanotic lesions with decreased PBF

A

TOF
Tricuspid/pulmonary atresia
Ebstein anomaly
DORV

61
Q

Cyanotic lesions with increased PBF

A

D-TGA/cc-TGA, TAPVR, Truncus ateriosis, DILV, HLHS

62
Q

What congenital heart defect is maternal lithium use associated with?

A

Ebsteins

63
Q

What syndrome is truncus arteriosus associated with

A

Di George- 30%

64
Q

Indications for 3x stage Fontan

A

Dominant RV: HLHS
Dominant LV: DILV, PA + intact VSD, Tricuspid atresia
Other Unbalanced AVSD, Complicated DORV (no PS)

65
Q

Stages of Fontan

A
  1. Norwood (1wk): Ao/PA shunt, BT shunt (RV-PA), Pulm banding if increased PBF, DKS if-
  2. Glenn (3-6mo): SVC to PA, removal BT shunt- when shunt fails/dec SpO2
  3. Fontan (2yrs): IVC to PA
66
Q

CHD associated with VACTERL

A

most commonly associated with VSD however ASD, hypoplastic left heart, transposition of the great arteries and tetralogy of Fallot also occur.

67
Q

CHD associated with Alagille (JAG/NOTCH)

A

Peripheral pulmonary stenosis (others include tetralogy of Fallot, septal defects, coarctation of the aorta)

68
Q

CHD associated with Williams (7q11.23del)

A

Supravalvular aortic stenosis (70% of cases), pulmonary valve stenosis

69
Q

ECG findings in LQT1 syndrome (KCNQ1)

A

Most common genotype- 35% LQTS
ECG: polymorphic VT (consistent with initial rhythm strip) classically triggered by exercise or emotional events.

69
Q

ECG findings in Brugada syndrome

A

Rare cause of SCD- defect in myocardial Na channels
‘coved’ ST elevation in V1/V2 and pseudo-RBBB.
Tachy-arrhythmias may be triggered by fever

70
Q

ECG findings in LQT2 syndrome

A

Second most common genotype (25-35%). Arrhythmia is classically triggered during sleep/rest
ECG: polymorphic VT

71
Q

D-TGA pathophys & repair?

A

5-7% of defects, M>F 3:1
Aorta from RV (cyanotic)
PA post from LV
- may have fixed/dynamic LVOT

Duct dependant- PDA, VSD, ASD/PFO

Sx: cyanosis at birth (does not respond to O2), tachypnoea, CCF within first few weeks, death <6mo if not treated
- If VSD/PDA more likely to develop CCF

No murmur unless VSD/LVOT, loud S2

ECH: R) axis/RVH/BVH
CXR: cardiomegaly, ^ PBF, ‘egg on a string’

Rx: PGE1- keep duct open
Surgery- Arterial switch
- May also need initial BT shunt if severe PS/subaortic stenosis = VSD

72
Q

Pathophys/Rx of L-TGA

A

L/cc-TGA 1% of patients
Ventricles switched
RA-LV (PA), LA-RV (Ao)

Physiologically normal but other associated abnormalities:
- 80% have VSD
- PS 50%, TR 30%
- AV block/SVT & reentrant tachy common
- Dextrocardia 50%
- Inverted CA

Asymptomatic unless other defects
May present in first few months if PS + VSD = cyanosis, large VSD = CCF

Murmur: nil, loud S2
If VSD; holosystolic LLSB
If PS: ESM RUSB
If TR/large VSD, apical rumble

ECG: absent Q waves V5/6, AV block, WPW

CXR: straight cardiac border

Rx: antiarrythmics/CCF rx
If PS+VSD - BT shunt
If large VSD - PA banding

May also need anatomic repair (Senning)/Fontan if single ventricle patho

73
Q

Cardiac lesions with increased risk of SVT/AVRT

A

cc-TGA, Ebsteins, HLHS, HOCM, Harmatoma (TS)

74
Q

Patho/Rx TOF

A

5-10% of cardiac defects (most common)

  • Large VSD
  • RVOT (infundibular stenosis 45%, pulmonary valve 10% or both 30%)
  • RVH
  • Overriding aorta
    (VSD & RVOT mainly contribute to pathology)
75
Q

Patho/Rx TOF

A

5-10% of cardiac defects (most common)

  • Large VSD
  • RVOT
  • RVH
  • Overriding aorta
76
Q

Well baby with continuous murmur at time of birth- Dx?

A

Coronary artery fistula
- 50% of CA abnormalities
- Can fistulate between heart/PA
- 90% terminate in R)heart (mimic ASD- ejection systolic murmur LUSB, split/fixed S2)
- PA - similar to PDA (wide PP, continuous murmur LUSB, LVH)
- LA - similar to MR (pansystolic murmur apex, LVH)
- LV- similar to aortic valve regurg (diastolic murmur LLSB)

PDA murmur NOT present at birth

77
Q

Lesions with prolonged PR

A

CHD: AVSD, Ebsteins
Acquired: ARF
Congenital heart block

78
Q

Lesions with superior axis

A

NATE (C)
Noonans- supravalvular pulm stenosis
AVSD/primum ASD
Tricuspid atresia
Ebsteins
CC-TGA

79
Q

Lesions with single S2

A

Abnormal valve:
- Obstructive: PS/AS/atresia/tricuspid atresia
- Eisenmengers/large VSD

Abnormal valve position:
- Truncus
- TOF
- TGA (both)
- HLH

+ severe PHTN

80
Q

Exam findings in PHTN?

A

RV heave
Narrowly split or single S2 (P2 closes early)
TR = holosystolic murmur
PR = early diastolic murmur
Hepatomegaly
Peripheral edema

81
Q

Presenting features of LQT1,2,3?

A

LQT1 (KCNQ1)/ Jervell and Lange-Nielsen syndrome– attacks during exercise/ swimming, broad based T waves
LQT2 (KCNH2) /Roman-Ward syndrome– response to sudden noise, low amplitude T waves
LQT3 (SCN5A) – attacks during rest/ sleep

82
Q

Murmur heard right infra-clavicular region, associated scar. Hx of cyanotic heart disease

A

BT shunt- stage 1 of Norwood procedure, redirects blood flow to lungs

83
Q

Continuous/machinery-like murmur at LUSE/left infra-clavicular, with bounding pulses.

A

PDA – persistent connection between aorta and pulmonary artery

84
Q

Pan-systolic, LLSE, harsh

A

VSD

85
Q

Crescendo-decrescendo ejection systolic in LUSE peaking in early/midsystole with fixed splitting of S2

A

ASD

86
Q

Long, harsh systolic murmur with cyanosis

A

TOF

87
Q

Blowing, holo-systolic at LLSE, increasing with inspiration and reducing with Valsalva

A

TR

88
Q

Holosystolic at the apex, radiates through to back or clavicular area (with
systolic click in MVP)

A

MR

89
Q

Qp:Qs >1

A

L > R shunt
Excess BF in lungs
- High arterial, low central venous O2

90
Q

Qp:Qs <1

A

R > L shunt
Excess BF in body (bypasses lungs)

91
Q

Qp:Qs <1

A

R > L shunt
Excess BF in body (bypasses lungs)
- Reduced tissue (arterial) oxygen delivery

92
Q

First, second and third most common valve to be affected in ARF?

A

Mitral (65-70% of patients)
Aortic valve (25%)
Tricuspid valve (10%)

93
Q

Causes single loud S2- features of Dx?

A

Abnormal position of arteries
(Cyanotic)
- Truncus
- Tricuspid atresia - LVH/superior axis
- TOF- BVH/RAD
- D-TGA- RAH/RVH
(Acyanotic)
- HLHS - RVH
- TOF- RVH/RAD
- cc/L-TGA- Q waves in RHS/limb leads

Abnormal PA/Ao
- Ao/PA stenosis
- Pulm atresia- RVH
- Large VSD/Eisenmenger

94
Q

Causes of prolonged PR

A

AVSD
Ebstein’s anomaly
Acute rheumatic fever
Congenital heart block

95
Q

Causes of WPW

A

Ebstein
Hamartoma (eg. TS)
HOCM
Single ventricle
ccTGA

96
Q

Causes of deep Q waves

A

HOCM
ccTGA (V1)
Anomalous L coronary artery (V5 + V6)

96
Q

Causes of deep Q waves

A

HOCM
ccTGA (V1)
Anomalous L coronary artery (V5 + V6)

97
Q

Dx ECG

A

sinus tachycardia and non-specific T-wave and ST-segment changes

QRS/QT prolongation
Low voltage QRS (<5mm in precordial leads)
Pathological Q waves
Ventricular arrhythmias (can be ectopics or VT)
AV block

98
Q

Dx ECG?

A

Large QRS due to hypertrophied muscle
T wave inversion/ST changes = unhealthy myocardium

99
Q

Dx ECG?

A

DCM- weak/floppy myocardium
- QT prolongation
- Low voltage QRS
- T/ST wave changes- unhealthy myocardium
- Ventricular ectopics/AV block

100
Q

Duration for prolonged QTc? + suggestive Hx?

A

In boys, a prolonged QTc is >450ms
In girls a prolonged QTc is >460ms.

Syncope, FHx SCD/long QT, meds (anticonvulsants/depressants/psychotics, ABx, antiemetics, antihistamines, antiarrythmics, antifungals)

Deafness- LQT5

101
Q

Dx this ECG?

A

Normal baseline EXG
Inherited condition affection Ca2+ influx channels, high adrenaline states unmask
- Exercise
- Stress

AVOID DEFIB/ADRENALINE

102
Q

Dx this ECG?

A

Brugada
- Inherited channelopathy
- Common in males/carb consuming cultures (Asia/Western)

103
Q

Dx this ECG?

A

ALCAPA- pathological Q waves 1, AVL, V6

104
Q

Causes hypertrophic CM (metabolic)

A

Lysosomal storage & mucopolysaccharidoses
- Hurler/Hunter
- I-Cell Disease

Glycogen storage diseases
-Pompe

105
Q

Causes dilated CM (metabolic)

A

Organic acidemias
- Homocysteinuria

FAO disorders
- MCAD

FRACP 2023 Cram Homicrons Edition (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions