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Cardio Week 6 Flashcards

1
Q

what is symptoms of valvular heart disease

A

chest pain, breathlessness, collapse/dizzy exertional symptoms

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2
Q

what kind of breathlessness are associated with valvular heart disease

A

orthopnoea (when lying flat) and paroxysmal noctural dyspnoea (patient wakes with sudden SOB)

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3
Q

what is apex beat in left ventricular dilation / hypertrophy

A

dilation - displaced and diffuse (volume overload)hypertrophy - heaving and displaced (pressure overload)

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4
Q

what is a murmur

A

audible turbulence of blood flow

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5
Q

what kinds of murmurs synchronise with pulse

A

systolic

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6
Q

what kinds of murmurs do not synchronise with pulse

A

diastolic

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7
Q

what is types of systolic murmurs

A

pan systolic - mitral regurgitationejection systolic - aortic stenosis

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8
Q

what is types of diastolic murmurs

A

early - aortic regurgitation mid - mitral stenosis

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9
Q

how should murmurs be described

A

systole or diastolewhat type or murmurwhere is it loudestwhere does it radiate towhat grade

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10
Q

what murmur radiates to carotids

A

aortic stenosis

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11
Q

what murmur radiates to axilla

A

mitral regurgitation

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12
Q

how to grade murmurs

A

I - very quiet II - quiet - easy to hearIII - loudIV - loud with thrillV - very loud with thrillVI - loud (audible without stethoscope)

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13
Q

right sided murmurs are louder with what?

A

inspiration

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14
Q

what is the characteristics of an innocent (functional) murmur

A

soft (less than 3/6 severity), position dependent, often early systolic (diastolic always pathological)

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15
Q

what is valve stenosis

A

valves do not open properly

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16
Q

what is valve regurgitation

A

valves do not close properly

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17
Q

what is investigations in murmur

A

non invasive - echoinvasive - cardiac catheterisation

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18
Q

causes of aortic stenosis

A

can be degenerative (age related), congenital (bicuspid valve) or rheumatic (previous rheumatic heart disease)

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19
Q

what is symptoms of aortic stenosis

A

breathlessness, chest pain (mimic angina but normal coronary arteries), dizziness, syncope

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20
Q

what is the treatment of aortic stenosis

A

valve replacement - preferrednew - TAVI (transcatheter aortic valve replacement - comorbidity, previous sternotomy) and BAV

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21
Q

what is features of mechanical valves

A

longevity, warfarin required, used in younger patients

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22
Q

what is features of bio-prosthetic valves

A

no warfarin, lasts 10 years, used in older patients

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23
Q

what is the causes of mitral regurgitation

A

leaflets (prolapse, rheumatic, myxomatous, endocarditis), chordae rupture (degenerative), papillary muscle rupture (ischaemic) or annular dilation

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24
Q

what is symptoms of mitral regurgitation

A

breathlessness, peripheral oedema, fatigue

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25
Q

what is signs of mitral regurgitation

A

displaced, tapping apexpansystolic murmer - axilla

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26
Q

what is the treatment of mitral regurgitation

A

diuretics and drugs for HF (ACE inhibitors)surgical - repair (prolapse) or replacement (degenerative)percutaneous - clips in infancy

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27
Q

what is main cause of mitral stenosis

A

rheumatic - congenital is rare

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28
Q

what is symptoms of mitral stenosis

A

breathlessness, fatigue, palpitations (AF)

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29
Q

what is signs of mitral stenosis

A

malar flush, tapping apex beat, mid diastolic rumbling, diastolic murmur localised to apex

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30
Q

what is the treatment of mitral stenosis

A

diuretics and treat AFsurgical - valve replacementballoon valvuloplasty

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31
Q

what is the causes of aortic regurgitation

A

leaflets (endocarditis, connective tissue diseases, rheumatic)annulus - marfans, aortic dissection

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32
Q

what is symptoms of aortic regurgitation

A

breathlessness

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33
Q

what is signs of aortic regurgitation

A

collapsing pulse, wide pulse pressure, displaced apex, early diastolic murmur left sternal edge

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34
Q

what is the the treatment of aortic regurgitation

A

medication - ACE inhibitors surgery - symptoms and LV dilation - valve replacement

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35
Q

what is the function of the placenta

A

fetal homeostasis, gas exchange, acid base balance, nutrient transport to fetus, waste product transport, hormone production, transport of IgG and PGE2

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36
Q

what are lungs like in foetus

A

fluid filled and unexpanded

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37
Q

what is liver like in foetus

A

little role in nutrition and waste management

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38
Q

what is the gut like in foetus

A

not in use

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39
Q

what is the foetal circulation

A

foetal heart pumps blood to placenta via umbilical arteriesblood from placenta returns to foetus via umbilical vein oxygenated, nutrient rich blood returns from placenta to right side of heart

40
Q

what 3 shunts are specific to foetal life

A

ductus venosus, foramen ovule, ductus arteriosus

41
Q

what is the role of the ductus venosus

A

connects umbilical vein to IVC - carries majority of placental blood straight into IVC by bypassing portal circulation

42
Q

what is the role of foramen ovale

A

opening in atrial septum connecting RA and LAallows best oxygenated blood to enter LA then LVmembrane flat on LA side

43
Q

what is the role of the ductus arteriosus

A

connects pulmonary bifurcation to descending aorta patency maintained by circulating PGE2 produced by placenta

44
Q

what are adaptations which foetus undergoes after birth

A

PVR decreases (reaches normal by 2-3 months)SVR increases (cord cut)more cardiac output to lungsforamen ovale closes (LA pressure exceeds RA)duct constriction - anatomical closure 7-10 days & ends up as fibrous ligament

45
Q

in which kind of babies does duct often fail to close

A

preterm treatment - wait and see, NSAIDs and surgery)

46
Q

if a congenital heart disease cause duct dependent circulation what can be done

A

IV prostaglandin E2 can be used to keep duct open until alternative shunt established or definitive surgery carried out

47
Q

what can happen if adaptation fails

A

persistent pulmonary hypertension more likely in sick babies - sepsis, hypoxic ischaemic insult, meconium aspiration syndrome, cold stress

48
Q

what is features of persistent pulmonary hypertension

A

lung vascular resistance fails to fall, shunts remain, blue baby, large difference between pre and post ductal O2 saturation

49
Q

what is treatment of persistent pulmonary hypertension

A

ventilation, oxygenation, drugs to make high systemic blood pressure, inhaled NO, ECLS (v severe cases)

50
Q

how does congenital HD present

A

screening - antenatal, newborn checkwell baby with clinical signs eg murmur unwell baby - cyanosis, shock or cardiac failure

51
Q

how does antenatal screening work

A

ultrasound at 18-22 weeks - 4 chamber view and outflow tract viewif disease - deliver in cardiac surgical centre or prostaglandin infusion if duct dependent lesion

52
Q

how does newborn screening work

A

around 24 hours - femoral pulses, heart sounds, murmurseg small murmur VSD (no haemodynamic consequences and may close spontaneously)

53
Q

which congenital HD signs presents soon after birth

A

cyanosis (deoxygenated blood either bypasses lungs and enters systemic or mixes with oxygenated and enters)eg transposition of great arteries

54
Q

which congenital HD signs presents 1-2 days after birth

A

murmurs, abnormal pulses, cyanosis

55
Q

what congenital HD signs presents 3-7 days after birth

A

sudden cardiac collapse, shock, cyanosis, sudden death

56
Q

what congenital HD signs presents 4-6 weeks after birth

A

signs of cardiac failure (reduced feeling, failure to thrive, breathlessness, sweatiness, hepatomegaly, crepitations)

57
Q

what congenital HD signs can present at 6-8 week GP check

A

incidental finding of murmurs at other clinical contacts

58
Q

what is the differential diagnosis of these signs

A

cardiac babies - blue with no resp distress (pre-post duct differential)resp - increased WOB, XR changesPPHN - otherwise very unwell babies (large pre-post ductal differential)

59
Q

what are examples of duct dependent conditions

A

duct dependent systemic circulation (hypopolastic left heart, critical aortic stenosis, interrupted aortic arch, critical coarctation of aorta)duct dependent pulmonary circulation (tricuspid atresia, pulmonary atresia)

60
Q

how does cardiac failure present

A

usually seen with moderate to large left to right shunts - increased pulmonary flow, increase ventricular load

61
Q

what is the long term management of major congenital HD

A

surgical management - repair vs pallitation developmental problems - hypoxia, bypass timeneed for further surgery - valves, stenosis or transplant emotional/social issues

62
Q

what kind of surgery can take place

A

patent ductus arteriosus repair (catheter), VSD repair or HLHS (3 stage complex surgery - ends with RV supplying systemic circulation)

63
Q

what are the two different kinds of inherited disease

A

channelopathies (mutations in genes that encode cardiac ion channels)cardiomyopathies (disease of heart muscle)

64
Q

what are 7 different types of channelopathies

A

congenital long QT syndrome, brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), short QT syndrome, progressive familial conduction disease, familial AF (in young ppl!!), familial WPW

65
Q

what is congenital long QT syndrome

A

QT interval >440 males, >450 femalesassociates arrhythmia - polymorphic VT (torsades de pointes), lone, AF, heart block

66
Q

what is the symptoms of CLQTS

A

syncope, SCD (sudden cardiac death) in children in young adults

67
Q

what is triggers of CLQTS

A

exercise, sleep, sudden noise, drugs, hypokalaemia

68
Q

what is the management of CLQTS

A

avoid QT prolonging drugs, correction of electrolyte abnormalities, avoidance of triggers

69
Q

what is brugada syndrome

A

risk of polymorphic VT, VFAF common ST elevation and RBBB in V1-V3

70
Q

what is genes associated with brugada syndrome

A

SCN5A and CACN1Ac

71
Q

what is triggers in brugada syndrome

A

sleep or rest, fever, alcohol, large meals

72
Q

what drugs should be avoided in brugada syndrome

A

anti-arrhythmic drugs, psychotropics, analgesics, anaesthetics

73
Q

what are the three different types of cardiomyopathies

A

hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (AVRC) and dilated cardiomyopathy

74
Q

what is hypertrophic cardiomyopathy

A

mutation in sarcomeric genes 1% CV mortality

75
Q

how can hypertrophic cardiomyopathy present

A

sudden death, heart failure, angina, atrial fibrillation, or can be asymptomatic

76
Q

what is arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

fibro-fatty replacement of cardiomyocytes autosomal dominant mutation in genes for desmosomal proteins; recessive in nondesomosomal genes

77
Q

what is dilated cardiomyopathy

A

sacromere and desmosomal genes, lamin A/C and desmin if connection disease, dystrophin if X linkedmales>females

78
Q

how is channelopathies and cardiomyopathies managed

A

diagnostic - clinical and genetic testingrisk management - lifestyle, pharmacological, non-pharmacoloicalfamily screening

79
Q

how may bacteraemic occur

A

patient specific reasons (poor dental hygiene, IV drug use, soft tissue infections) or associated with procedures (dental treatment, IV cannulae, permanent pacemaker)

80
Q

what are the predisposing factors in endocarditis

A

rheumatic HD, mitral valve prolapse, IVDU (tricuspid lesion), prosthetic valves, congenital HD, hypertrophic cardiomyopathy

81
Q

what organisms occur in the mouth

A

alpha haemolytic strep -viridans (50% of cases)

82
Q

what organisms occur in native and prosthetic valve

A

staph aureus and staph epidermis strep viridans less common and occurs later (>60 days) post valve surgery

83
Q

what organisms occur in prolonged hospitalisation

A

enterococci (gut)

84
Q

what organisms occur in IVDU

A

staph aureus

85
Q

what is high clinical suspicion in endocarditis

A

new valve lesion/regurgitant murmur, embolic event of unknown origin, sepsis of unknown origin, haematuria, glomerulonephritis, suspected renal infarction, fever

86
Q

what is other symptoms of endocarditis

A

anorexia and weight loss, splinter haemorrhage, clubbing, splenomegaly, olsers nodes, janeways lesions and roth spots

87
Q

what are olsers nodes

A

red-purple, raised tender lumps with pale centre fingers and toes occur at any time of endocarditis and last from hours to several days

88
Q

what are janeway lesions

A

non tender, often haemorrhagic and occur mostly on palsm and soles (base of thumb and little finger)last days to weeks acute endocarditis

89
Q

what are roth spots

A

retinal haemorrhages with white or pale centres

90
Q

what investigations are used in endocarditis

A

blood cultures - at least 3 sets of samples (6 bottles)serological tests can be sent if diagnosis suspected but blood negative FBC (normochronic, normocytic anaemia is common)U&Es, LFTs (Alk phos raised) CRP (raised in any infection)m urine (proteinuria and haematuria)Echo CXR

91
Q

treatment of clinical endocarditis, culture results awaited, no suspicion of staphylococci

A

penicillin and gentamicin

92
Q

treatment of suspected staphylococcal endocarditis (IVDU, recent IV devices or cardiac surgery)

A

vancomycin and gentamicin

93
Q

treatment of streptococcal endocarditis

A

penicillin and gentamicin

94
Q

treatment of enterococcal endocarditis

A

ampicillin/amoxicillin and gentamicin

95
Q

treatment of staphylococcal endocarditis

A

vancomycin or flucloxacillin or benzylpenicillin and gentamicin

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