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RACP 2023 > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Cardiac catheter: what happens to O2 concentrations when:

  • ASD
  • VSD
  • PDA
  • Above with Eisenmengers
A

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2
Q

Cardiac catheterisation in restrictive CM vs constrictive pericarditis

A

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3
Q

Cardiac catheterisation in HOCM vs AS

A

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4
Q

What happens to PV loop when:
- DCM
- LVH
- AS
- MS
- AR
- MR
- positive ionotropy
- incr/decr afterload

A

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5
Q

CAD treatment: when invasive vs medical?

A

Medical: Stable CAD

PCI: uncontrolled symptoms on medical, pt wish (outcomes = better angina relief)

CABG: L main, triple vessel including prox LAD, 2/3 vessel with LV dysfunction

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6
Q

Tx of angina

A

BB
CCB
CTN patch/ISMN
Nicorandil

Perhexilline: inhibits cartinine palmitoytransferse –> mteabolism of glucose instead of FAs –> more efficient
- careful Caucasians 6-10% poor metabolisters
- CYP2D6
- peripheral neuropathy

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7
Q

Arrhythmias post MI?

A

VF
AIVR: ectopic pacemaker
AV block: SA node affected in RCA block

cMRI best predictor

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8
Q

LV aneurysm presentation?

A

cardiac failure
persistent ST elevation
stroke

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9
Q

LV rupture presentation?

A

tamponade
heart failure

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10
Q

Which arteries supply which parts of the heart?

A

Inferior Right coronary
Anteroseptal Left anterior descending

Anteroapical Left anterior descending (distal)
Anterolateral Circumflex

Posterior Right coronary artery

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11
Q

Wellen’s: describe

A

Deep T in V2-V3
Or biphasic T waves
Indication of critical stenosis in LAD

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12
Q

Cardiac pathology of rheumatic heart disease?

A

Aschoff bodies: granulomas
Anitschkow cells: macrophages

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13
Q

When to intervene in rheumatic MS?

A

Small MVA
Symptomatic

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14
Q

Cardiac arteries from RCA + LCA?

A

LCA
§ Circumflex
§ LAD
§ L marginal
RCA
§ Right ant ventricular
§ Right marginal
§ Posterior intraventricular artery
§ SA nodal branch in 60% of cases
§ AV nnodal branch 80% cases

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15
Q

SA/AV node action potential?

A

Slow influx Na
Fast influx Ca
Slow outflow K

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16
Q

Ventricular AP?

A

Fast Na influx
Slow Ca influx
K outflow
Refractory period

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17
Q

Conduction system: describe from SA –> Purkinje

A

SA –>AV ring (held there) –> AV node –> Bundle of His –> R and L branches –> moderator band –> Purkinje

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18
Q

Alpha 1 and 2 receptors: effect

A

Alpha 1: Vasocontriction
Alpha 2: venoconstriction

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19
Q

Beta 1 and 2 receptors: effect

A

Beta 1: HR, contractility, conduction increased

Beta 2: smooth muscle relaxation

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20
Q

Indications for PM?

A

-SND: pace only if symptomatic - there is no too slow
- Dual chamber

  • AV block: pace even if asymptomatic in 2nd degree type 2, high degree AB block, CHB
  • otherwise only asymptomatic
    • Dual chamber
  • LBBB: more likely to have underlying structural heart disease
  • HIS bundle pacing: RV pacing can worsen LVEF in LV dysfunction
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21
Q

ICD indications?

A
  1. Secondary
    Patients who have experienced a previous sudden cardiac arrest or ventricular arrhythmia
  2. Primary
    Patients who have not previously experienced sudden cardiac arrest or ventricular arrhythmia, but are at risk
    1. Patients at least 40 days post-MI LVEF ≤ 35% NYHA class II or III
      LVEF ≤ 30% NYHA class I
      LVEF ≤ 40% non-sust VT, inducible VT/VF at EPS
  3. Non-ischemic patients
    LVEF ≤ 35%
    NYHA class II or III
    “DANISH study”-NEJM Sept 2016 –no mortality benefit in NICM patients (subgp analysis <70yrs benefit)
  4. Patients at risk of SCA due to genetic disorders
    Long QT syndrome
    Brugada syndrome
    Hypertrophic cardiomyopathy (HCM)
    Arrhythmogenic right ventricular cardiomyopathy (ARVC)
    Catecholaminergic polymorphic VT
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22
Q

CRT indications?

A
  • Left ventricular systolic dysfunction: EF ≤35%
    • Wide LBBB ≥150ms
      Class 2 to ambulatory class 4 heart failure symptoms
    • QRS > 120
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23
Q

Rheumatic heart disease affects which valves?

A

Aortic
Mitral
Tricuspid

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24
Q

Pathology in RHD?

A

Aschoff bodies: granulomas with giant cells
Anitschkow cells: macrophages with wavy nucleus

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25
Q

When do you start anticoagulation in a patient with rheumatic MS and AF?

A

CHADS VASc does not apply –>anticoagulate

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26
Q

When to intervene in Rheumatic MS? CI?

A

Severe stenosis <1.5cm and symptomatic

Not surgical candidate OR pliable valve: PMBC
Is: MV surgery

Exertional symptoms

Asymptomatic but PASP > 50 or new AF

CI: NO CLOT

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27
Q

DEFIB Indications?

A
  • No clear reversible cause
    • long QT syndrome
    • arrhythmogenic right ventricular dysplasia
    • hypertrophic obstructive cardiomyopathy
    • Cardiac sarcoidosis
    • previous cardiac arrest due to VT/VF
    • previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
    • Heart failure + reduced LVEF
    • Brugada syndrome
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28
Q

Antiarrhythmic classes?

A

1: Na channel blockers (1a quinidine procainamide) (1b lidocaine phenytoin) (1c flecanide propafenone)
4: Ca (Verapamil, Diltiazem)
3: K (amiodarone, sotalol)
2: BB (propanol, metoprolol)

Fleicanide has no effect on ventricle

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29
Q

Digoxin MoA?

A

Slows heart rate and reduces AV nodal conduction by an increase in vagal tone and a reduction in sympathetic activity.

Increases the force of myocardial contraction by increasing the release and availability of stored intracellular calcium.

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30
Q

Amiodarone MoA?

A

Decreases sinus node and junctional automaticity, slows atrioventricular (AV) and bypass tract conduction and prolongs refractory period of myocardial tissues

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31
Q

Adenosine MoA?

A

Causes transient heart block in AV node
Causes hyperpolarisation: increases outward K flux

32
Q

Ivabradine MoA?

A

inhibits a current regulating the interval between depolarisations of the sinoatrial (SA) node.
- Blocks influx of Na –> reduction in AP slope
It reduces heart rate (by about 10 beats/minute) which in turn lowers cardiac workload and myocardial oxygen demand.

33
Q

Antiplatelets MoA? and significant SE’s

Dypyridamole
Aspirin
Ticag
Clop/prasugrel
Tirofibran

A

Dypyridamole
Non specific phophodiesterase inhibitor that decreases cellular uptake of adenosine
- Antiplatelet and vasodilating properties

Apirin
Inhibition of COX 1 + 2
- THROMBOXANE inhibitors indirectly

Ticagrelor
P2Y12 receptor blocker (activates platelets usually)
- Better than clopi
○ Reducing CV death, MI, stroke without incr in bleeding risk
- Reversible
CI: due to buildup of adenosine
- 2nd/3rd AV block
- asthmaCOPD

Clopi/ PRASUGREL
Metabolites inhibits binding of ADP to platelet P2Y12 receptor
- ADP unable to bind to glycoprotein GPIIb/IIA which inhibits platelet aggregation
- Irreversible

Tirofibran (T for 2)
Glycoprotein Iib/IIIa inhibitors

34
Q

CPVT genetics?

A

RYR2 gene: MAJORITY
* Gain of function mutation
* Calcium channel ion
* Autosomal dominant inheritance
Rare –> CASQ2 gene (autosomal recessive inheritance)

35
Q

CPVT features?

A

Bidirectional VT
Induced by exercise/stress

36
Q

CPVT treatment?

A

BB
ICD

37
Q

ARVC mutaitons?

A

Autosomal dominant

Desmoglein
Plakkophil

Cardiac desmosomal proteins

38
Q

ARVC features?

A

Exercised induced
Can sometimes have thick skin, curly hair
ECG: epsilon wave, TWI V1-V3

39
Q

Brugada syndrome features?

A

SCN5A LOSS mutation: Na channel, sometimes Ca and K
ECG: coved ST, inducible VT, syncope, family history cardiac death

40
Q

Brugada management?

A

ICD
Treat fevers
Catheter ablation

41
Q

Long QT features (1,2,3)

A

K channel in 1,2 Na channel in 3

1: exercise, young males
2: emotion/ auditory: females
3: sleep, males > 18

42
Q

Greatest risk of SCD in LQT?

A

QRS > 500

43
Q

Treatment LQT

A

BB
ICD

44
Q

Use of flueicanide/ ajmaline challenge?

A

Given NA channel blocker (fleicanide) if suspected clinically in Brugada type 2/3
○ Converts it to type 1

45
Q

What can be used in LQT as a provocation challenge?

A

Adrenaline

46
Q

Indications for ICD?

A
  1. Secondary
    Patients who have experienced a previous sudden cardiac arrest or ventricular arrhythmia
  2. Primary
    Patients who have not previously experienced sudden cardiac arrest or ventricular arrhythmia, but are at risk
    1. Patients at least 40 days post-MI LVEF ≤ 35% NYHA class II or III
      LVEF ≤ 30% NYHA class I
      LVEF ≤ 40% non-sust VT, inducible VT/VF at EPS
    2. Non-ischemic patients
      LVEF ≤ 35%
      NYHA class II or III
      “DANISH study”-NEJM Sept 2016 –no mortality benefit in NICM patients (subgp analysis <70yrs benefit)
  3. Patients at risk of SCA due to genetic disorders
    Long QT syndrome
    Brugada syndrome
    Hypertrophic cardiomyopathy (HCM)
    Arrhythmogenic right ventricular cardiomyopathy (ARVC)
    Catecholaminergic polymorphic VT
47
Q

Fe replacement effect on CCF?

A

MPROVES SYMPTOMS AND QOL
REDUCES HOSPIRALISATIONS
DOES NOT IMPROVE MORTALITY
HAS TO BE IV –> ORAL HAS MINIMAL EFFECT

Fe failure strongly assoc with incr mortality

48
Q

Indications for ionotropes in CCF

A

If symptoms/sign of peripheral hypoperfusion + BP < 90mmHg

* Increases mortality regardless of agent  Take off ASAP
49
Q

Indications for CRT?

A

Class II - IV CCF

wider QRS = better remodelling = more likely to have symptomatic response

PREVENTS ARRHYTHMIC DEATHS

50
Q

Treatment for HEFpEF

A

Low dose spironolactone
SGLT2

51
Q

Heart transplant complications?

A
  • First 30 days
    ○ Graft failure
    • 6-12 months
      ○ Opportunistic infections
    • After 1 year
      ○ Vasculopathy
    • Beyond 5 years
      • Lymphoma + other malignancies common
51
Q

Heart transplant complications?

A

BIGGEST CAUSE OF DEATH = CAS

   - First 30 days
	○ Graft failure
- 6-12 months
	○ Opportunistic infections 
- After 1 year
	○ Vasculopathy
- Beyond 5 years
    - Lymphoma + other malignancies common
52
Q

DCM CAUSES?

A

Ischemic
Infectious
- Parvovirus
- Herpes
- Influenza
Toxins
- Alcohol
- Cocaine
CTD
Hypothyroidism
Muscular dystrophy
HTN
Infiltrative
- Haemachromatosis
- Sarcoidosis
Metabolic disorders
Mitochondrial disorders
Syndromal
- Alstrom
- Barth syndrome

Peripartum CM

53
Q

DCM gene associations?

A

TTN: TITIN gene (autosomal dominant)
LMNA gene

54
Q

DCM treatment?

A

ICD/CRT
Heart failure medications
Treat arrhythmias

55
Q

Restrictive CM: sign of poor prognosis?

A

Syncope

56
Q

How to differentiate restrictive CM with constrictive pericarditis?

A

Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis
* prominent apical pulse
* absence of pericardial calcification on CXR
* the heart may be enlarged
* ECG abnormalities e.g. bundle branch block, Q waves

57
Q

CM investigations: what do you see?

A

ECHO: bilateral atrial enlargment, severe diastolic dysfunction
- Increased early diastolic filling to Atrial filling ratio

Cardiac catheter: increased ventricular diastolic pressure

Sr protein electrophoresis: Ig light chain amyloidosis

58
Q

Factor most predictive of SCD in HOCM?

A

Septal thickness > 30mm

59
Q

How does HOCM examine?

A

Related to valve-septum interaction: mitral regurgitation

Systolic cresc decresc murmurs
- Best heard at L lower sternal border
Increased intensity with swuating –> standing / Valsalva

60
Q

ECG + echo signs of HOCM? Which one is most specific?

A

ECG:
- q waves in I, aVL, V5-6 + inferior (II III aVF) leads
- LVH
- Non specific T wave changes in lateral leads
○ Progressive T wave inversion
- Episodic AF/ VT

ECHO:
- systolic anterior motion of mitral valve, asymmetric hypertrophy , LVOT obstruction
- Septum >15mm proband = MOST SPEICFIC SIGN
- LVH typically asymmetric
Non dilated LV with L/R hypertrophy

61
Q

Which drugs worsen HOCM?

A

Ionotropes
Diuretics
Vasodilators
ACE

62
Q

Indications for ICD in high risk patients?

A
  • Sudden death in first degree relative
    • Sustained VT
    • Unexplained syncope
    • Abnormal BP response to exercise
    • NSVT
    • Resuscitated sudden death event
      • LV thickness > 30mm
63
Q

HOCM management?

A
  • Amiodarone
  • Beta-blockers or verapamil for symptoms
  • Cardioverter defibrillator
    • Only one to prevent death
  • Dual chamber pacemaker
64
Q

Aortic dissection management?

A
  • Type A (ascending aorta): surgery
    • Type B (descending aorta): medical therapy: control HR + reduce HR, pain control
      ○ Beta blocker (1)
      ○ CCB, ACEI (2)
      ○ AVOID HYDRALAZINE
      § INCREASES STRESS ON SORTIC WALL
65
Q

Aortic aneurysm: when to intervene?

A

Ascending: > 55m
BAV with risk factors (Fox, HT, coarctation, growth > 3-5mm year): >50 mm
Marfan: > 50mm
Loeys Dietz: > 42
Turner: > 27mm

66
Q

FH:
- most common sign?
- are females protected?
- genetic mutations?

A
  • most common sign: corneal arcus
  • are females protected: pre menopausal ONLY
  • genetic mutations: LDL, PCSK9, ApoB100
67
Q

What is Eisenmenger syndrome?

A

When L –> R becomes L –> R
pHTN –> RVH –> pressure becomes greater

68
Q

Outcome for adults with small VSD?

A

often high rate of sport closure in early years
good prognosis if NO ventricular dilatation/ pHTN

69
Q

Which syndrome is AV septal defect assoc with

A

Downs

70
Q

Disorders that can cause EIsenmenger’s

A

ASD
VSD
PDA

71
Q

Which syndromes are PS associated with?

A

Noonan
William

72
Q

Tetralogy of Fallot

A

VSD
Overriding aorta
RVH
PS

73
Q

Bicuspid aortic value associations

A

Turners

74
Q

When to intervene on Aortic aneurysm

A

> 55 ALL PATIENTS
50 MARFANS
45 MARFANS + risk factor

RACP 2023 (17 decks)

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