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
When do you start anticoagulation in a patient with rheumatic MS and AF?
CHADS VASc does not apply -->anticoagulate
26
When to intervene in Rheumatic MS? CI?
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
27
DEFIB Indications?
* 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
28
Antiarrhythmic classes?
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
29
Digoxin MoA?
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.
30
Amiodarone MoA?
Decreases sinus node and junctional automaticity, slows atrioventricular (AV) and bypass tract conduction and prolongs refractory period of myocardial tissues
31
Adenosine MoA?
Causes transient heart block in AV node Causes hyperpolarisation: increases outward K flux
32
Ivabradine MoA?
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
Antiplatelets MoA? and significant SE's Dypyridamole Aspirin Ticag Clop/prasugrel Tirofibran
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
CPVT genetics?
RYR2 gene: MAJORITY * Gain of function mutation * Calcium channel ion * Autosomal dominant inheritance Rare --> CASQ2 gene (autosomal recessive inheritance)
35
CPVT features?
Bidirectional VT Induced by exercise/stress
36
CPVT treatment?
BB ICD
37
ARVC mutaitons?
Autosomal dominant Desmoglein Plakkophil Cardiac desmosomal proteins
38
ARVC features?
Exercised induced Can sometimes have thick skin, curly hair ECG: epsilon wave, TWI V1-V3
39
Brugada syndrome features?
SCN5A LOSS mutation: Na channel, sometimes Ca and K ECG: coved ST, inducible VT, syncope, family history cardiac death
40
Brugada management?
ICD Treat fevers Catheter ablation
41
Long QT features (1,2,3)
K channel in 1,2 Na channel in 3 1: exercise, young males 2: emotion/ auditory: females 3: sleep, males > 18
42
Greatest risk of SCD in LQT?
QRS > 500
43
Treatment LQT
BB ICD
44
Use of flueicanide/ ajmaline challenge?
Given NA channel blocker (fleicanide) if suspected clinically in Brugada type 2/3 ○ Converts it to type 1
45
What can be used in LQT as a provocation challenge?
Adrenaline
46
Indications for ICD?
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
Fe replacement effect on CCF?
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
Indications for ionotropes in CCF
If symptoms/sign of peripheral hypoperfusion + BP < 90mmHg * Increases mortality regardless of agent Take off ASAP
49
Indications for CRT?
Class II - IV CCF wider QRS = better remodelling = more likely to have symptomatic response PREVENTS ARRHYTHMIC DEATHS
50
Treatment for HEFpEF
Low dose spironolactone SGLT2
51
Heart transplant complications?
- First 30 days ○ Graft failure - 6-12 months ○ Opportunistic infections - After 1 year ○ Vasculopathy - Beyond 5 years - Lymphoma + other malignancies common
51
Heart transplant complications?
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
DCM CAUSES?
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
DCM gene associations?
TTN: TITIN gene (autosomal dominant) LMNA gene
54
DCM treatment?
ICD/CRT Heart failure medications Treat arrhythmias
55
Restrictive CM: sign of poor prognosis?
Syncope
56
How to differentiate restrictive CM with constrictive pericarditis?
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
CM investigations: what do you see?
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
Factor most predictive of SCD in HOCM?
Septal thickness > 30mm
59
How does HOCM examine?
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
ECG + echo signs of HOCM? Which one is most specific?
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
Which drugs worsen HOCM?
Ionotropes Diuretics Vasodilators ACE
62
Indications for ICD in high risk patients?
- Sudden death in first degree relative - Sustained VT - Unexplained syncope - Abnormal BP response to exercise - NSVT - Resuscitated sudden death event - LV thickness > 30mm
63
HOCM management?
* Amiodarone * Beta-blockers or verapamil for symptoms * Cardioverter defibrillator - Only one to prevent death * Dual chamber pacemaker
64
Aortic dissection management?
- 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
Aortic aneurysm: when to intervene?
Ascending: > 55m BAV with risk factors (Fox, HT, coarctation, growth > 3-5mm year): >50 mm Marfan: > 50mm Loeys Dietz: > 42 Turner: > 27mm
66
FH: - most common sign? - are females protected? - genetic mutations?
- most common sign: corneal arcus - are females protected: pre menopausal ONLY - genetic mutations: LDL, PCSK9, ApoB100
67
What is Eisenmenger syndrome?
When L --> R becomes L --> R pHTN --> RVH --> pressure becomes greater
68
Outcome for adults with small VSD?
often high rate of sport closure in early years good prognosis if NO ventricular dilatation/ pHTN
69
Which syndrome is AV septal defect assoc with
Downs
70
Disorders that can cause EIsenmenger's
ASD VSD PDA
71
Which syndromes are PS associated with?
Noonan William
72
Tetralogy of Fallot
VSD Overriding aorta RVH PS
73
Bicuspid aortic value associations
Turners
74
When to intervene on Aortic aneurysm
>55 ALL PATIENTS > 50 MARFANS >45 MARFANS + risk factor