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2 - Diseases Of The Human System > Chronic CV Diseases - 2 > Flashcards

Chronic CV Diseases - 2 Flashcards

1
Q

What are cardiac arrhythmias?

A

disorders of heart rate

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2
Q

What are the fast (tachy) arrhythmias?

A
  • atrial fibrillation
  • ventricular tachycardia
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3
Q

What are the slow (Brady) arrhythmias?

A
  • heart block
  • Drug induced! (b blocker, digoxin)
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4
Q

What is the most common cause of pulse around 50bpm?

A

drug induced
- beta blocker

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5
Q

What is heart block and what are the 3 classifications ?

A
  • slow/no conduction through the AV node to ventricles of impulse from SA node
  • Prolonged p-q interval on ECG
  • Mild delay: Signals get through slowly (1st degree).
  • Some blocks: Occasional skipped beats (2nd degree).
  • Complete block: Needs pacemaker (3rd degree).
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6
Q

How do fast heart rates impair cardiac function?

A
  • reduced diastolic filling time therefore reducing cardiac output and leading to heart failure
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7
Q

What is the difference in ECG between atrial and ventricular tachyarrhythmia?

A

atrial - narrow ORS, no P wave
ventricular - broad strange QRS

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8
Q

Why is ventricular tacharrthymia dangerous?

A

leads to ventricular fibrillation and death

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9
Q

What are cardiac pacemakers used to treat?

A

BRADYARRHYTHMIAs

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10
Q

What do cardiac pacemakers do?

A
  • Don’t ‘pace’ the heart if natural heart rate is above a certain level – e.g. 50 bpm
  • Maintain a minimum heart rate by providing electrical stimulation.
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11
Q

What are the risks of pacemakers?

A

theoretical risk of electrical interference – causes sensing to shut down

  • electrical fields - MRI, electrosurgery/diathermy
  • dental equipment THEORETICAL risk only
  • Pulp Testers OK - avoid INDUCTION scalers though – these generate strong EM field
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12
Q

What do the waves of a sinus rhythm signify?

A
  • P wave – atrial depolarisation
  • QRS complex – Ventricular
    depolarisation
  • T wave – Ventricular repolarisation
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13
Q

What is ventricular fibrillation usually caused by?

A
  • Heartattack
  • Electrocution
  • Long QT syndrome–can be drug induced
  • Wolf-Parkinson-Whitesyndrome
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14
Q

How can ventricular fibrillation be treated?

A
  • Treat with ‘Defibrillation’
  • Implanted defibrillators used in risk cases
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15
Q

What is ventricular fibrillation?

A
  • No cardiac output - Death follows!
  • Electrical heart activity but disorganised
  • muscle fibres contracting in ventricles at random – no emptying of ventricle
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16
Q

What is asystole?

A
  • No cardiac output
  • No electrical activity
  • Defibrillation not possible (adrenaline used)
  • Low chance of survival
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17
Q

When should congenital heart defects be suspected?

A

with ANY body congenital defect (Cleft Lip/Palate, Downs)

18
Q

What are the types of congenital heart defects?

A
  • ATRIAL septal defects
  • VENTRICULAR septal defects
  • Patent ductus arteriosus
  • Great vessel malformations
19
Q

In what diseases is finger clubbing seen?

A
  • Cardiac disease
  • Lung diseases
  • Inflammatory Bowel diseases
  • Liver cirrhosis
20
Q

What is the value for cyanosis?

A

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

21
Q

Central VS Peripheral Cyanosis

A

Central
Congenital heart disease, lung diseases etc
Poor oxygenation of the blood
Oxygenated and deoxygenated mixing
Mucosa and tongue blue

Peripheral
Cold environment
Slow circulation due to vasoconstriction
Oxygen levels fine
Raynauld’s disease

22
Q

How can you test congenital defects?

A

doppler ultrasound scan

23
Q

What are qualities of atrial septal defect?

A
  • Most remain undetected throughout life
  • Low risk of endocarditis except in IVDA (drug) patients
  • Usually non-cyanotic
24
Q

What are the qualities of ventricular septal defect?

A
  • Higher endocarditis risk
  • Higher risk of long term heart failure
  • Usually non-cyanotic
  • Different types present – commonest is in the muscle between the ventricles
25
Q

How can septal defects close?

A
  • Some shrink naturally with time and require no intervention
  • Open heart surgery and closure directly of the defect via patch
  • Catheter insertion of a mesh on each side of the defect by arterial access
26
Q

What is co-artctation of the aorta?

A

narrowing of the aorta just after the carotid artery on the left side has exited. this restricts blood flow to systemic arteries of lower body

birth defect

27
Q

What is a patent ductus arteriosus?

A

ductus fails to close leading to turbelent blood flow and increased endocarditis risk

28
Q

What is infective endocarditis?

A

infection of the endocardium usually on the valves

29
Q

What organisms is mainly implicated in infective endocarditis?

A

oral steptococci (viridans)

30
Q

What is vegetation formation?

A

Microbial colonisation of thrombi on endocardial surface abnormalities causes areas of thickening and stiffening of the valves

31
Q

What is the cycle of infective endocardiditis

A

surface abnormalities (inflammation) > haemodynamic changes > turbulence > platelet / fibrin deposition (thrombus) > vegatation > microbial attacgment and multiplication > enlargement of vegetation

32
Q

What is the effect of infective endocarditis?

A

Prolonged antibiotic treatment (intravenous)
- 4+ weeks of bacteriocidal treatment
- - Often combinations of drugs

Cardiac valve damage
- Valve dysfunction
- Urgent valve replacement needed

33
Q

Which dental procedures are a risk?

A

Procedures involving manipulation of the dento-gingival junction and causing a bacteraemia
* Extractions
* Periodontal therapy
* Gingival surgery
* Implants
* Restorations
* Only if the gingival margin involved or matrix used

34
Q

What is bacteraemia?

A

viable bacteria in the blood

35
Q

What do the NICE guidelines say 2008 for antibiotic prophylaxis?

A

NO indication for Antibiotic Prophylaxis
No indication from literature of benefit
Possible harm from Adverse Drug Reaction

36
Q

What should dental efforts be concentrated towards? (via NICE GL 2008)

A

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

  • Improve patient’s oral hygiene efforts
  • Remove areas of dental sepsis
  • – unrestorable carious teeth, teeth causing infection
  • Work at prevention of oral disease
  • Diet, hygiene, high fluoride content toothpaste
37
Q

Who are the highest risk patients that may require AB prophylaxis?

A

o Previous endocarditis
o Valve replacement surgery
o Certain congenital heart defects

38
Q

What happens to surviors of infective endocarditis?

A

significantly reduced length & quality of life

39
Q

When is prophylaxis used?

A

Only for procedures likely to produce a significant bacteraemia
* MANIPULATION OF DENTO-GINGIVAL JUNCTION

40
Q

What does the montgomery ruling require for consent to prophylaxis?

A

“Montgomery” requires:

  • Consequences of ABP must be discussed
  • Consequences of NO ABP must be discussed
  • For cases who are ‘high risk’ undergoing invasive dental procedures – dento-gingival manipulation.
41
Q

What consititues a dentally fit patient?

A

minimal oral sepsis (active caries)
no endodontic disease
no periapical/dontal disease

2 - Diseases Of The Human System (19 decks)

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