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BDS2 BAMS > Valves, Malformations and Endocarditis > Flashcards

Valves, Malformations and Endocarditis Flashcards

1
Q

4 cardiac valves

A

left (aortic and mitral)

right (pulmonary and tricuspid)

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2
Q

higher pressure cardiac valves

A

left (aortic and mitral)

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3
Q

lower pressure cardiac valves

A

right (pulmonary and tricuspid)

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4
Q

what valves more commonly fail

A

left (aortic and mitral)

- under higher pressure

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5
Q

2 ways left heart valves may fail

A

Aortic stenosis & incompetence

  • Narrowed - restrict blood flow into aorta during systole,
  • increasing work flow of ventricle

Mitral stenosis & incompetence
- Not closed properly – blood flow back in

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6
Q

how aortic stenosis and incompetence leads to left heart valve failure

A
  • Narrowed - restrict blood flow into aorta during systole,

- increasing work flow of ventricle

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7
Q

how does mitral stenosis and incompetence lead to left heart failure

A

Not closed properly – blood flow back in

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8
Q

what is key to cardiac valve disease treatment

A

replace valve with prosthetic valve before permanent damage to heart

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9
Q

cardiac valve anatomy

A

Cusplets of collagen

Tied onto muscle wall of heart

Fibres connecting valves onto papillary muscles
- Papillary muscles designed to keep valves under tension

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10
Q

how can MI cause a valve to fail

A

damage to muscle - can cause valve to fail (acute valve failure)

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11
Q

valve stenosis

A

Not opening = build-up of pressure in left atrium, reduction in CO, higher pressure in pulmonary system

e.g. mitral valve (atrium to left ventricle)

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12
Q

mitral valve

A

left atrium to ventricle

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13
Q

tricuspid valve

A

right atrium to right ventricle

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14
Q

pulmonary valve

A

right ventricle to pulmonary artery

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15
Q

aortic valve

A

left ventricle to aorta

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16
Q

prevalence of cardiac valve disease

A

very common in the elderly and Downs
(Elderly - don’t notice as activity low)

  • Breathless on exertion
  • Tired
    but rarely any symptoms - undiagnosed!
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17
Q

4 causes of aortic valve disease

A

Congenital abnormality

  • Bicuspid aortic valve
  • Formed the valve incorrectly when developing
  • Can be in teens and 20s and need valve replaced

Myocardial infarction
- papillary muscle rupture

Rheumatic Fever
- Immunological reaction to streptococci

Dilatation of the aortic root 
- Syphilis 
- Aneurysm formation
Stretch – valves pulled apart 
To do with disease of aorta not valve
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18
Q

congenital abnormality leading to cardiac valve disease

A

Bicuspid aortic valve

  • Formed the valve incorrectly when developing
  • Can be in teens and 20s and need valve replaced
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19
Q

how can MI lead to cardiac valve disease

A

papillary muscle rupture

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20
Q

how does rheumatic fever lead to cardiac valve disease

A

Immunological reaction to streptococci

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21
Q

how can dilation of aortic root lead to cardiac valve disease

A

Stretch – valves pulled apart
To do with disease of aorta not valve

  • Syphilis
  • Aneurysm formation
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22
Q

investigating valve disease

A
  • Previously stethoscope

* Ultrasound

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23
Q

what is seen in an ultrasound investigation of heart

A

Realtime heart moving
- See valves open and close and muscle contracting

Easy to see where issue is
- Can identify moving liquid moving though heart
(Coloured for different flows; Red correct direction - through the valve)
- should have unidirectional flow

Doppler valve assessment?
- Quantity of problem

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24
Q

2 options for valve replacements

A

mechanical valve (e.g. ball and socket)

pig valves (porcine)

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25
Q

mechanical valves

A

made of metal in workshop

need to be on anticoagulants
- Blood will clot on unless use anticoagulant
need to follow SDCEP anticoagulant guidance for dental care

risk of endocarditis

  • Maximise Oral Health
  • Be sensitive to patient and surgeon needs
  • Be aware of international disagreement in this area
  • Sometimes antibiotics are given – case by case
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26
Q

advantages of pig valve

A

right size (similar heart size)

Natural valve leaflets (normal collagen)

Blood won’t stick to them anymore than they do in pig (no anticoagulant needed, e.g. children would have bleeding problem as fall over often)

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27
Q

disadvantage of pig valve

A

Pig valves last less (10 years) tissue will wear out, natural wear as removed from environment

  • Fine for elderly as longer than life expectancy of patient (save anticoagulant complication)
  • Not issue in child - by 20 get a proper metal valve which will last 30 years
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28
Q

when would you use a pig valve and mechanical valve

A

Pig valves - extremes of life

Longevity - metal valve

Every time replace - risk of death only want 2/3 in lifetime

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29
Q

what are congenital heart defects

A

Failure of normal development and fusion of embryonic heart
- Often undetected & asymptomatic

Suspect in ANY congenital defect (CLP, Downs)

  • Any child with congenital defect is high risk of having higher risk of congenital cardiac malformation
  • Not worked somewhere so likely multiple issues in genetics
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30
Q

when do congenital heart defects occur

A

Happen as you are forming as an embryo

Cardiovascular forms from 2 parallel circuits combine with 1 heart with 2 effective sides

  • A lot join together or are separated
  • May not work well
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31
Q

4 types of congenital heart defects

A

ATRIAL septal defects

VENTRICULAR septal defects

Patent ductus arteriosus

Great vessel malformations

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32
Q

when does the join between pulmonary artery and aorta need to shut

A

when you breath

Usually first half hour of before, after 1-2 days no blood going to pulmonary circulation from aorta

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33
Q

what happens when there is over fuse of atria

A

hole right to left side of atria, low pressure system so doesn’t notice blood going back to lungs
(common)

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34
Q

atrial septal defects

A

from one atria to another

Oxygenating the blood twice, no issues if volume of blood low

On X-Ray see

  • Swelling on right side of heart (left of pic)
  • Sticks close to spine usually
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35
Q

ventricular septal defects

A

Move blood from left to right side

Some left ventricle blood into pulmonary artery (normally aorta), then into lungs

  • Left ventricle needs to work more to maintain CO as losing proportion through right ventricle
  • Leads to heart failure unless managed
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36
Q

normally left ventricle contracts

A

squirt out aorta

37
Q

normally right ventricle contracts

A

squirt into pulmonary artery

38
Q

process of ventricle septal defect leading to right sided heart failure

A

blood into aorta and right ventricle and pump into lungs again,

increasing workload of right side (higher pressure system)

lead to right side failure
(less common, picked up and lower activity tolerance need to repaid before damage)

39
Q

ductus arteriosus

A

runs from pulmonary artery to aorta
- Allows blood in fetus to move from right ventricle to aorta

Lungs expand on breath

  • Easier blood to go through lungs then into aorta
  • Ductus needs to close
40
Q

ductus arteriosus allows

A

blood in fetus to move from right ventricle to aorta

Lungs expand on breath

  • Easier blood to go through lungs then into aorta
  • Ductus needs to close
41
Q

closing of ductus arteriosus causes

A

co-arctation of aorta

closing carries onto aorta - so closed ductus and narrowed aorta
- Hard to pump to rest of body

Right arm BP normal, left arm low - arm artery coming off after narrowing
- Can live with but can lead to heart failure as more work

42
Q

patent ductus arteriosus

A

Blood flow opposite direction
- Need to shut off

Remains open - aorta into lungs
- Like venricle septal defect

43
Q

dental impact of congenital heart abnormaltiies

A

may have endocarditis risk

Guidance from Cardiologist required

  • Check with cardiologist for infection risk in dental treatment
  • case by case basis

Most are mild and undetected!

44
Q

infective endocarditis

A

Infection of the endocardium
- Usually on the valves

Microbial colonisation of thrombi on endocardial surface abnormalities
- Many organisms implicated

45
Q

number of new endocarditis cases each year

A

1400 (UK)
- 20 deaths

50% patients over 50

46
Q

is there predisposing factors of endocarditis?

A

often none

  • Rheumatic fever less common now
  • Prosthetic valves more common now
47
Q

7 physical findings for diagnosing infective endocarditis

A

Fever 90%

Heart murmur 85%

Embolic phenomena e.g. splenic or renal infarction, cerebral emboli >50%

Skin manifestations e.g. Osler nodes, spliner haemorrhages and petechiae 18-50%

Splenomegaly 20-57%

Septic complication e.g. pneumonia, meningitis 20%

Mycotic (infective) aneurysm 20%

48
Q

3 organisms in infective endocarditis

A
  • Streptococci
  • Staphylococci
  • Fungi
49
Q

effect of infective endocarditis

A

Prolonged antibiotic treatment

  • 4+ weeks of bactericidal treatment
  • Often combinations of drugs

Cardiac valve damage

  • Valve dysfunction
  • Urgent valve replacement needed?
50
Q

when is prevention of infective endocarditis possible

A

if ‘at risk’ patients identified in dentistry

  • Medical history
  • Prominent identification in case record
51
Q

possible preventions of infective endocarditis

A

Avoid risk procedures?

Use antibiotic prophylaxis when needed?
NICE Guidelines 2008 – Review in 2015
Review of available evidence
- NO indication for Antibiotic Prophylaxis in literature of benefit
- Possible harm from ADR
Advise that Antibiotic Prophylaxis can be used in special circumstances

52
Q

evidence of antibiotic prophylaxis not used in infective endocarditis prevention

A

NICE states that AB prophylaxis is ineffective
- not recommended routinely

ESC & AHA suggest that it is for highest risk patients

53
Q

prevalence of infective endocarditis and morality

A

2150 cases of IE in UK annually
Incidence is rising

Up to 20% IE patients die on 1st admission – up to 50% overall

Up to 45% attributed to S. viridans

Survivors will have significantly reduced length & quality of life

54
Q

dental role in infective endocarditis

A

Consequences of ABP must be discussed
Consequences of NO ABP must be discussed
- Advise high risk patients about the evidence for and against

Patient to discuss with cardiac team
- Dentist informed of decision

55
Q

3 dental theorectical issues if prophylaxis is recommended

A

Is procedure to be performed ‘high risk’

Is patient wanting prophylaxis

What does SDCEP recommend in these circumstances

56
Q

drug regime for infective endocarditis

A

Amoxycillin 3g oral 1hr before procedure – even if used recently

UNLESS ALLERGIC
Clindamycin 1.5g
Higher ADA risk – ONLY use if penicillin allergic

57
Q

4 pointers of advice for reducing patient risk

A

Attendance for oral care

Rapid management infection

Maximal oral hygiene and prevention

Avoiding risk activity - piercings

58
Q

central cyanosis caused by

A

congenital heart disease

59
Q

peripheral cyanosis caused by

A

cold environment

60
Q

when does cyanosis exist

A

when there is 5g/dl or more of deoxygenated Hb in the blood

May have Hb of 15 but only 10 carry O2
- Hard to get oxygen to tissues

need to fix or will become a permanent issue

61
Q

signs of central cyanosis

A

Go blue
- Peripherally shut down
- Circulation to peripheral tissues will stop
- Blood will become saturated
Cyanosis throughout body including those with lots of blood flow (core tissues)
- Tongue, oral mucosa (usually always pink)

Finger clubbing
- Swelling of terminal digits of fingers

62
Q

what is infective endocarditis

A

Infection of the endocardium
- Usually on the valves

Microbial colonisation (bacteria) of thrombi on endocardial surface abnormalities 
- Platelets to adhere to damaged endothelial surfaces and allowing vegetative build up

Many organisms implicated
- mainly oral streptococci
DENTAL PROCEDURES implicated in the cause

63
Q

what main organisms are implicated in infective endocarditis

A

Many organisms implicated
- mainly oral streptococci
DENTAL PROCEDURES implicated in the cause

64
Q

example of poor antibiotic prescription in dentistry

A

Dentists had poor understanding of the differing risks that cardiac problems had for endocarditis.
- Many patients came to expect antibiotics before dentistry - even thought it was unnecessary

Example: Rheumatic Fever – a condition commonly leading to prophylaxis pre 2008

However only those patients who had HEART VALVE DAMAGE from the condition (Rheumatic Heart Disease) actually needed prophylaxis. Usually this was Mitral valve disease (Small number)
- few dentists made this distinction or arranged Echocardiograms to see.

It was easier just to give an antibiotic before the dental procedure – just in case

65
Q

cycle of infective endocarditis starting with surface abnormalities

A

surface abnormalities

haemodynamic changes

turbulence

platelet/fibrin deposition (thrombus)

vegetation
- as thrombus colonised by bacteria in blood

microbial attachment and multiplication
- enlarged and cause damage to tissue and endocardium

enlargement of vegetation

66
Q

physical findings in diagnosis of endocarditis

A

Flu like then develop murmur/splint/haemorrhage, onset can be 6 weeks post procedure – hard to link

Physical findings

  • Fever
  • Heart murmur
  • Embolic phenomena e.g. renal/splenic infarction, cerebral embol
  • Skin manifestations e.g. Osler nodes, splinter haemorrhages and petechiae
  • Splenomegaly
  • Septic complications e.g. pneumonia, meningitis
  • Mycotic (infective) aneurysm
67
Q

effect of infective endocarditis

A

Prolonged antibiotic treatment

  • 4+ weeks of bactericidal -treatment IV treatment
  • Often combinations of drugs

Cardiac valve damage

  • Valve dysfunction
  • Urgent valve replacement needed?

Significant risk of Death from disease or its complications

68
Q

how is prevention of infective endocarditis possible in dentistry

A

Prevention only possible if ‘at risk’ patients identified in dentistry
- From the Medical history
(Many had no previous history of endocardia issue)
- Prominent identification in case record (Susceptible to multiple episodes once had one)

69
Q

what to do once find an ‘at risk’ of infective endocarditis in dentistry

A

Avoid risk procedures?
- Removing all teeth – not ideal

Use antibiotic prophylaxis when needed?

  • Complicated prophylaxis protocols
  • —Divide pt into risk categories
  • —Oral or IV depending on perceived risk
70
Q

2006 guidelines Tx for antibiotic prophylaxis dental treatment

A

Antibiotic prophylaxis for dental procedures may be supplemented with

  • chlorhexidine gluconate gel 1% or chlorhexidine gluconate mouthwash 0.2%, used 5 minutes before procedure
  • —no evidence
71
Q

3 high risk cardiac failures requiring AB Prophylaxis according to BSAC 2006

A

High risk cardiac failures requiring antibiotic prophylaxis

  • Previous infective endocarditis
  • Cardiac valve replacement surgery i.e. mechanical or biological prosthetic valves
  • Surgically constructed systemic or pulmonary shunt or conduit
72
Q

dental procedures requiring antibiotic prophylaxis according to BSAC 2006

A

Dental procedures requiring antibiotic prophylaxis
- All dental procedures involving dento-gingival manipulation

Patients given AMOXYCILLIN and GENTAMYCIN IV before dental treatment which meant treatment had to be delivered in general hospital setting

73
Q

5 types of cardiac patients that are not at risk of infective endocarditis

A

Coronary Artery Bypass Grafting

Angioplasty & Stent

Hypokinetic cardiac muscle (following an MI)

Implanted Pacemaker

Implanted Defibrillator

74
Q

4 dental treatments that are at risk of infective endocarditis

A

INVOLVE DENTO-GINGIVAL MARGIN MOVEMENT

Extractions

Periodontal therapy

Implants (surgical)

Restorations
- If gingival margin involved or matrix used

75
Q

2 dental procedures that are not at infective endocarditis risk

A

Endodontics
- Instrumentation in root canal only

Impressions

76
Q

what was the impact on the NICE guidelines in 2008 on AB prophylaxis

A

prior AB prophylaxis used for patients with very low or no risk and exposing patients to treatment protocols and antibiotics that were not necessary

NO indication for Antibiotic Prophylaxis
- No indication from literature of benefit
- Possible harm from ADR (adverse drug reaction to antibiotic)
But: Is the lack of evidence the same as evidence of no risk

77
Q

post 2008 dental efforts to reduce infective endocarditis focussed on

A

Dental efforts to be concentrated on reducing risk by reducing size and frequency of oral bacteraemia

  • Develop every time eat, chew, brush teeth
  • Small bacteraemia are frequent and normal throughout the day
78
Q

3 dental orientated methods to reduces oral bacteraemis

A

Improve patient’s oral hygiene efforts
-Areas of plaque trapping and oral bacteria habitat can be removed as efficiently as possible

Remove areas of dental sepsis
- unrestorable carious teeth, teeth causing infection
Work at prevention of oral disease

Diet, hygiene, high fluoride content toothpaste

79
Q

why was their controversy after the 2008 NICE guidelines

A

European and US Guidelines different than NICE

Cardiac Surgeons unhappy
- wanted antibiotics for some surgical groups – mainly valve replacements

Cardiologists less unhappy
- Valve pt in particular at unnecessary risk

Patients confused

80
Q

consequences of NICE prophylaxis guideline review in 2015

A

NICE states that AB prophylaxis is ineffective

ESC & AHA (American and European) suggest that it is effective for the highest risk patients (divided pt population)

  • Previous endocarditis
  • Valve replacement surgery
  • Certain congenital heart defects
2150 cases of IE in UK annually 
- Incidence is rising 
- Up to 20% IE patients die on 1st admission – up to 50% overall 
Up to 45% attributed to S. viridans 
- Dental cause

Survivors will have significantly reduced length & quality of life

81
Q

recent 2015 review of NICE prophylaxis guidelines looked at

A

Groups at risk of developing infective endocarditis

Interventional procedures associated with risk of infective endocarditis should not use AB Prophylaxis
- Including dentistry

levels of bacteraemia
- regular bacteraemia reduced as much as possible

Prophylaxis regimen to be used

82
Q

risks of prophylaxis use compared to none (NICE guidelines)

A

small risk and small death chance

NICE Guidance could potentially lead to increase number of pt having endocarditis and increase deaths
- Led to doctors and pts realising current guidance unmaintainable for UK

think of picture of outweighing risks

83
Q

what was changed in the reviewed 2016 NICE Guidelines on prophylaxis

A

“Antibiotic prophylaxis against infective endocarditis is not recommended routinely”

Allow for situations where clinical need would outweigh guidance
- remained the same but with greater degree of flexibility

Guidance can be taken or not
- many NHS trusts take literally – dentists discourage from giving AB Prophylaxis even in extreme situations

84
Q

Dental issues arisen due to NICE prophylaxis guidelines

A

How do I determine which patients should be offered AB prophylaxis?
- Didn’t help determine how should and shouldn’t

NICE gives no recommendation on which dental procedures should be covered

NICE gives no advice on the prophylaxis regime to be used

85
Q

what are the SIPCEP prophylaxis guidelines for all dental team

A

Practical recommendations

Includes:

  • Patient selection for discussion (Patients at risk)
  • How to advise a patient
  • —–Importance of GENERAL oral health measures, Seek guidance from surgeon
  • What antibiotic regime to give if decided by the patient & doctor
  • What dental procedures to cover
86
Q

Montgomery issues for informed consent for prophylaxis

A

Consequences of ABP must be discussed

Consequences of NO ABP must be discussed

For cases who are ‘high risk’ undergoing invasive dental procedures – dentogingival manipulation.

Pt fully aware of both sides, see evidence and decide themselves

87
Q

how should the decision regarding prophylaxis be carried out

A

Made by patient and their physician

Communicated to dentist in writing

Only for procedures likely to produce a significant bacteraemia
- E.g. MANIPULATION OF DENTO-GINGIVAL JUNCTION

Prophylaxis given if pt wished
- Dentist is to implement pt wishes whatever they may be for appropriate dental procedures

Pt risk assessed on Mx History
Discuss with physician and communicate pt wishes to dentist
So prophylaxis can be used when wanted for appropriate dental procedures

88
Q

most effective ways at preventing infective endocarditis in dentistry are (4)

NICE Guidelines 2008

A

All the advice about reducing patient risk STILL applies.

  • Attendance for oral care
  • Rapid management infection
  • Maximal oral hygiene and prevention
  • Avoiding risk activity – piercings
89
Q

drug regime for AB prophylaxis

A

Amoxycillin 3g oral 1hr before procedure – even if used recently, Unless allergic
- In surgery so can control any reaction that occurs

Clindamycin 1.5g
- Higher ADA risk – only use if penicillin allergic

BDS2 BAMS (54 decks)

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