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Cardiology Flashcards

1
Q

Classes of pulmonary hypertension

A

Type 1: Isolated pre-capillary
Type 2: Left heart disease
Type 3: Lung disease
Type 4: Pulmonary artery obstruction (CTEPH)
Type 5: Obscure mechanisms

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2
Q

Initial echo finding in PAH

A

Peak tricuspid regurgitation velocity >2.8 suggestive of possible pulmonary hypertension

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3
Q

RHC findings in group 2 and 5

A

PCWP >15mmHg
MPAP >20
Group 2: PVR <2WU

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4
Q

RHC findings in groups 1, 3, 4, 5

A

PCWP <15mmHg
MPAP >20
PVR >2WU

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5
Q

Causes of group 1 PAH

A

Idiopathic 50-60%
Connective tissue diseases
Congenital heart disease
Portal hypertension
10% heritable
Drugs: dasatinib, meth
Genetics
HIV a risk factor
Schistosomiasis leading cause in third world

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6
Q

Gene implicated in PAH

A

BMPR2 gene mutations associated with 20% risk of developing PAH
Gene usually inhibits smooth muscle proliferation and induces apoptosis
Mutation causes proliferation of pulmonary vascular cells
Younger age of onset, more severe, increased mortality

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7
Q

High risk features in PAH - 20% 1 year mortality

A

Signs of right heart failure
Rapid progression
Repeated syncope
BNP >800 or NT-Pro-BNP >1100
RA area >2.6cm2
Moderate or large pericardial effusion

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8
Q

General measures in PAH

A

Supervised exercise program
Psychosocial support
Immunisation
Diuretics
O2 if PaO2 <60mmHg
Correct iron levels if IDA
Anticoagulation no longer routinely indicated

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9
Q

Acute vasodilator response in PAH

A

Give inhaled NO, iloprost or IV epoprostenol
if mPAP drops by >10 to below 40 without decrease in CO/CI then positive test = responder
Treat with CCB (<10% are responders)

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10
Q

Treatment of PAH with cardiac comorbidities

A

Start with mono therapy ERA or PDE5i

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11
Q

Treatment of PAH low/intermediate risk

A

Start dual therapy ERA and PDE5i

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12
Q

Treatment of PAH high risk

A

Start triple therapy ERA, PDE5i and PCA.
After 3-6 months if no improvement consider changing PDE5i to riociguat and/or change PCA to selexipag

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13
Q

Endothelin-1 receptor antagonists

A

Bosentan: both A and B antagonist. 10% hepatotoxicity
Ambrisentan: selective A antagonist. Less hepatotoxic, possible worsen ILD in IPF
Macitentan: Both A and B antagonist.
Nasopharyngitis and anaemia

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14
Q

Drugs targeting NO pathway

A

Sildenafil/tadalfil
-Increase intracellular cAMP and cGMP –> pulmonary vasodilation
No mortality benefit known

Riociguat
-Vasodilator stimulating soluble guanylate cyclase
-Benefit in CTEPH
-Not use in combo with PDE5i as increased hypotension and death

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15
Q

Drugs targeting prostacyclin pathway

A

Prostacyclin analogues
Epoprostenol IV
-Most potent pulmonary vasodilator
-Used for progressive disease and RHF
Iloprost inhaled

Selexipag
-Oral non-prostatnoid prostacyclin receptor agonist
-Add on therapy if ERA/PDE5i does not result in improvement after 3-6 months

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16
Q

Management of patients in high risk category on triple therapy not improving

A

Add on IV epoprostenol and refer for lung transplant

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17
Q

ECG finding most suggestive of VT?

A

AV dissociation

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18
Q

Differentiating SVT and VT

A

ABCDE
A - axis - north west
B - broad - >200msec VT
C - concordance - lack of QRS complexes in V1-6 = VT
D - AV dissociation
E - early part of QRS - R wave upstroke is <40msec in SVT and >40msec in VT

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19
Q

Cardiac sarcoid

A

Most commonly presents as heart block
Echo: wall motion abnormalities +/- thinning in a non-coronary distribution
PET and CMR required
-Reverse perfusion pattern seen on PET

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20
Q

Long QT syndrome

A

Autosomal dominant
70-80% will have positive genetic test
LQT1 - provoked by exercises
LQT2 and 3 - provoked by lack of sleep
Beta blocker for all
-Most effective in LQT1
IVD if refractory to beta blocker or very high risk

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21
Q

Brugada

A

Autosomal dominant
Mutations in cardiac sodium channel SCN genes (SCN5 most common)
SCD in 4th decade
Inv: ECG and rule out structural changes
Types 1 and 2 pattern
If type 2 to drug challenge (flecainide) to see if type 1 can be provoked
Arrythmias more common at night/whilst sleeping
Not secondary to exercise
Premature ventricular beats can provoke VF

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22
Q

Brugada management

A

Treat fevers promptly
Avoid alcohol and cocaine
Screen 1st degree relatives
ICD if high risk
Observe if Brugada pattern type 2 (not syndrome), asymptomatic, and no FHx of SCD

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23
Q

Mobitz II

A

No PR prolongation
High risk of progression to CHB
PPM if symptomatic, or if asymptomatic but very bradycardic

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24
Q

Complete heart block

A

PPM unless asymptomatic and rate >40 - can observe
Poor prognosis if associated with anterior MI

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25
Arrythmogenic right ventricular cardiomyopathy/dysplasia
Anatomy: RV dilatation/dysfunction Histology: fibrofatty infiltration of myocardium Arrhythmias: monomorphic VT most common with LBBB pattern Pathogenesis: Impaired desmosome function when subjected to mechanical stress Exercise plays a key role in disease development Genetic: 30% familial, defects in a variety of genes
26
ARVD management
Avoid rigorous exercise and competitive sports Long-acting cardioselective beta blocker - metoprolol XR Indications for ICD: -cardiac arrest -Symptoms due to VF/VT -Documented VF/VT -Low LVEF <35% -Syncope likely due to VF/VT If metoprolol not working --> sotalol --> amiodarone or flecainide --> cardiac transplant
27
Amyloidosis
Extracellular deposits of fibrils Deposit as beta pleated sheets Congo red stain --> apple green birefringence Present with HFpEF, low voltage ECG, AF, increased wall thickness on echo High BNP poor prognosis
28
AL amyloidosis
primary - associated with plasma cell dycrasias. heart involved 50% of the time and is main determinant of prognosis Periorbital purpura Treat with chemo +/- SCT
29
AA amyloidosis
secondary - due to RhA, IBD, chronic infection
30
ATTR amyloidosis
Wild type or inherited Causes cardiomyopathy and/or neuropathy (sensory and autonomic neuropathy, carpal tunnel) Atrial deposits correlate with AF Common cause of heart failure in the elderly Different TTR mutations correlate with severity CMR then 99m technetium pyrophosphate scintigraphy scan NYHA I to III - Tafamidis Liver +/- heart transplant options
31
Management of cardiac amyloid
Diuretics mainstay Beta blockers poorly tolerated as patients rely on heart rate for output due to fixed low stroke volume ACE-i poorly tolerated due to profound hypotension CCBs contraindicated Anticoagulation if AF, thrombi or embolic events Liver +/- heart transplant in h-ATTR
32
Hypertrophic cardiomyopathy
Most common inherited cardiomyopathy Autosomal dominant Abnormal hypertrophy, LV outflow tract obstruction, diastolic dysfunction ECG most sensitive Treat HF, beta blockers, avoid diuretics and digoxin as worsen obstruction, alcohol septal ablation/surgery if severe obstruction, AICD to prevent SCD, screen first degree relatives
33
Ebstein's anomaly
Apical displacement of tricuspid valve Can occur with ASD, VSD, P.S Accessory pathway and arrhythmias common Surgical repair for adults with TR when HF symptoms present, worsening exercise tolerance, progressive RV systolic function
34
Cardiac conditions that require surgical antibiotic prophylaxis
Prosthetic valves Previous I.E Congenital heart disease if unprepared cyanotic defect or repaired defect with residual defect near prosthetic material RHD in indigenous Australians Consider in heart transplant patients
35
Amiodarone mechanism of action
Potassium channel blocker Type 3 antiarrhythmic
36
Amiodarone side effects
Hepatotoxicity Thyroid toxicity (Hypo and hyper) Pulmonary toxicity Occular toxicity (photosensitivity 50%, corneal deposits 90%)
37
Verapamil and digoxin
Higher digoxin concentrations
38
Indications for AF ablation
Symptoms refractory to medical management Ablation does not improve outcomes in general population Does not alter indications for anticoagulation In HFrEF - improves EF, reduces mortality and reduces hospitalisation in those with EF <35%
39
Beta blockers in heart failure
Bisoprolol, nebivolol, metoprolol succinate are cardioselective Carvedilol is B1, B2 and A1 blocker - better for hypertensive pts Dizziness and dyspnoea are early side effects which generally improve In asthma use cardioselective beta blocker if <15% reversibility, otherwise contraindicated. Fairly well tolerated in COPD Benefits are dose dependent
40
Ivabradine
Slows down sinus node firing rate -Won't be effective if in AF Improves mortality and sudden cardiac death No substitute for beta blocker however can be used if: -HR remains high >70 despite max dose bb -Asthma contraindicating bb use -BB are not tolerated
41
ACE-i in heart failure
Benefit in all groups Improves mortality but not sudden cardiac death ARBs - benefits greatest in ACE naive patients
42
ARNI
Cause a fall in NT-Pro-BNP but rise in BNP (BNP is a neprolysin substrate) Add to therapy if NYHA II-IV and LVEF <40% after 3-6 months adequate therapy Must wait 36 hours after stopping ACE before commencing due to risk of angioedema
43
SGLT2 in HFpEF
Similar efficacy in diabetics and non-diabetics Best in LVEF >50% Driven by decreased hospitalisations. No mortality benefit
44
ASD
Most common congenital abnormality in adults Assoc. with L to R shunt --> volume overload of R side Can develop pulmonary vascular disease - depends on size and duration of shunt
45
Findings in ASD with significant shunt:
RV heave Wide, fixed splitting of second heart sound Pulmonary outflow murmur
45
Management of ASD in adulthood
Without PH -If significant heamodynamic shunt --> closure If moderate PH --> consider closure If severe PH --> no closure If paradoxical embolism --> closure SCUBA diving contraindicated Pregnancy: increased risk if history of supraventricular arrhythmia or RV failure
45
VSD
2nd most common abnormality in childhood but only accounts for 10% in adulthood due to spontaneous closure Characteristic holosystolic murmur Membranous type most common Risk of large VSDs: progressive pulmonary vascular disease, Eisenmengers, HF, arrythmias, I.E Close if: Haemodynamic significant shunt, progressive AR due to VSD, consider if history of I.E. Do not close if Eisenmengers present
46
Pulmonary stenosis
Associated with Noonan syndrome Pulmonary balloon valvuloplasty
47
Patent ductus arteriosus
Associated with prematurity and maternal rubella "Machinery" murmur Closure if left-side cardiac chamber enlargement as long as the pulmonary artery pressure is <50% of systemic
48
Metastatic cardiac tumours
Melanoma, thymoma, germ cell tumour Treat underlying neoplasm Surgery if obstructive symptoms
49
Malignant cardiac tumour
Angiosarcoma most common malignant tumour Typically arise in RA and assoc. with pericardial effusion Present with SOB and chest pain Most die within 6-12 months, 2 years with surgery
50
Benign cardiac tumours
Atrial myxoma most common, usually LA attached to fossa ovalis Mean age 50 after an embolic event Surgery if mitral valve obstruction to decrease rates of embolic events Papillary fibroelastoma usually on surface of aortic or mitral valve Present late - 8th decade Surgery if embolic symptoms
51
PCSK9 inhibitors
Evolucumab/alivocumab PCSK9 usually binds to LDL-c receptor on hepatocytes targeting it for degradation Monoclonal Abs reduce the activity of PCSK9 Reduce LDL by 61%/1.9mmol. 79% of patients achieved target of <1.8 LDL. Improved MACe Inclisiran (siRNA) binds to the RNA-induced silencing complex to cleave mRNA encoding for PCSK9 resulting in decreased hepatic production of PCSK9 Given 0, 3, 6 months then every 6 months so less often
52
Tetralogy of Fallot features
VSD RV outflow obstruction Overriding aorta RV hypertrophy
53
Coarctation genetic syndrome association
Turner syndrome
54
ASD closure - measurement used
pulmonary-to-systemic blood flow (shunt) ratio >1.5:1 Closure contraindicated if PAH present
55
ASD genetic syndrome association
Down syndrome and Holt-Oram syndrome
56
VSD genetic syndrome association
Down syndrome
57
Most specific echo sign of severe AR
Holodiastolic flow reversal in descending aorta
58
Ebstein's anomaly main pathology and associations
50% chance of WPW and ASD Also have severe TR because of the apical displacement of the tricuspid valve

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