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Human Diseases > W15 55 cardiac conditions requiring surgical intervention and their dental implications > Flashcards

W15 55 cardiac conditions requiring surgical intervention and their dental implications Flashcards

1
Q

What are the signs of heart disease?

A

Peripheries - temperature (HF pt cold to touch), capillary refill time, corneal arcus, xanthelasma, cyanosis, oedema, clubbing
Pulse
Heaves and thrills
Heart sounds

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2
Q

What are some symptoms of heart disease?

A

Chest pain
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
(Pre-) syncope
Palpitation
Ankle swelling

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3
Q

What are common heart conditions causing chest pain?

A

Angina pectoris - myocardial ischaemia (chest pain relating to the heart)
Pericarditis pain - pericardial inflammation
Pleuritis pain - pleural inflammation

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4
Q

What is the CCS classification of angina?

A

I - angina on strenuous prolonged exertion
II - slight limitation of ordinary activity eg walking or climbing upstairs rapidly
III - marked limitation of ordinary activity
IV - discomfort/pain with any physical activity or at rest

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5
Q

What pain does angina cause?

A

Constricting discomfort in chest, neck, shoulders, jaw or arms

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6
Q

What is pericarditic pain?

A

Sharp, stabbing pain, quick onset, relieved by leaning forward, exacerbated by lying flat or deep breathing

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7
Q

What is pleuritis pain?

A

Sharp, stabbing chest pain occurring at a set point upon inspiration

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8
Q

What is ankle swelling an indication of?

A

Right heart failure - back pressure

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9
Q

Through Starlings forces, how does ankle swelling occur? (Pg532 img)

A

Pressure in the right heart at the end of diastole is higher, causing back pressure through the capillaries. This rises capillary hydrostatic pressure, so more of a shift of fluid outside the capillaries in the interstitial tissues than in capillaries themselves.

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10
Q

What is dyspnoea indicative of?

A

Suggestive of ischaemia or heart failure (or both)

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11
Q

How does dyspnoea occur?

A

Due to left ventricle failing to increase output during exercise —> pulmonary venous pressure (back pressure) —> pulmonary oedema
Oedema increases the distance for gas exchange to occur, so it occurs slower, with CO2 rising, giving the feeling of breathlessness.

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12
Q

Is oxygen a treatment for dyspnoea?

A

Dyspnea is very more commonly hypercarbonaemia than hypoxia, so oxygen is not a treatment for dyspnoea.

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13
Q

What happens if diabetic patients complain of dyspnoea?

A

It’s identical to them talking about chest pain (because diabetic neuropathy means they don’t feel chest pain in the same way), they probably have angina

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14
Q

What happens to Starling’s curve in health vs heart failure? (PG533 GRAPH)

A

Preload = volume in heart at end of diastole (end of receiving the blood)
As you increase preload, (as EDV increases), SV increases. Plateaus in a healthy individual.
In heart failure, preload will increase but stroke volume will go down.

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15
Q

Why does orthopnoea occur?

A

Redistribution of blood from legs to lungs
Increases left-ventricular pre-load, decreased vital capacity and decreased pulmonary compliance

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16
Q

What is preload?

A

Volume in heart at the end of diastole

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17
Q

Why does paroxysmal nocturnal dyspnoea occur? (mechanism not well understood)

A

Left ventricle suddenly unable to match output of right ventricle
Likely due to adrenergic activity during sleep. Also a manifestation of sudden left HF.

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18
Q

What is pre-syncope vs syncope?

A

Pre-syncope is dizziness, lightheadedness, visual disturbance, muscular weakness
Syncope is loss of consciousness

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19
Q

How does syncope happen in a fixed cardiac output state?

A

Syncope occurs due to a reduction in cerebral perfusion
Patients will severe aortic stenosis = narrowing of aortic valve. Have a thick stroke volume eg 50ml as opposed to a healthy 70ml. Rate dependent, if can’t increase HR anymore, and you put more physical demand on them, they will become pre-syncope
Pacemaker dependent patients - stops you from going lower than a HR of a certain pulse. Can’t match exercise demands so if you want to run the pacemaker won’t go higher.

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20
Q

How can syncope happen due to a sudden loss in vascular resistance?

A

Syncope occurs due to a reduction in cerebral perfusion
Eg Suddenly going from cold to hot, or something frightens them etc.

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21
Q

How do cardiac output, stroke volume, heart rate and mean arterial blood pressure relate to perfusion?

A

CO = SV X HR
MAP = CO X SVR
Tissue perfusion requires flow and pressure. Perfusion is a state where you are providing nutrients. Needs a pressure gradient and flow to restore that gradient.

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22
Q

What is palpitation?

A

Awareness of heartbeat - fast, irregular, heavy, pauses

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23
Q

What can temperature indicate for peripheral perfusion?

A

Cool = poor blood flow
Hot = increases blood flow (vasodilated) - often septic patients

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24
Q

What can capillary refill time indicate for peripheral perfusion?

A

Pressure on thumb nail until skin blanches, release and count how long to refill
Normal = <2s
Very abnormal >6s

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25
Q

What can peripheral cyanosis indicate for peripheral perfusion?

A

(Blue around edges)
High oxygen extraction from the blood - poor blood flow

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26
Q

Signs of hypercholesterolaemia

A

Corneal arcus - white ring around the iris
Xanthalasma - fatty deposits under eyelids

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27
Q

How is severity graded for oedema?

A

Height - ankle, mid-calf, sacral, nipples (probably very unwell eg HF)
Water retention - water follows the sodium

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28
Q

By what mechanism does oedema occur?

A

Eg in myocardial dysfunction like ischaemia heart disease, there is a decrease in DV
This activates RAAS, retaining salt and thus water
Increases circulating volume
Stretches the heart more (in health this will meet with the increased SV), but dysfunctional hearts will lead to worse HF
(Thus drugs acting on RAAS system can help treat HF)

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29
Q

What else does SV lead to according to Le Plass’s law?

A

Decreased SV leads to an increase LV diastolic volume and pressure
This changes the shape of the heart, eg thickness and geometry, ventricular remodelling
When increasing muscle muscle of the heart, it increases the oxygen demands since more muscle is doing work, and also increases stiffness and compliance, and thus pressures further feeding back into the loop of dysfunction
(the law explains how increasing pressure or volume in heart leads to adverse heart remodelling).

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30
Q

What should pulse be at different ages?

A

Rate - should be 50-100 in an adult
Upto 160 when younger but down to 100 by age 5

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31
Q

What can different pulses indicate?

A

Character:
Normal
Slow rising - aortic stenosis
Water hammer - aortic regurgitation

Volume - felt centrally (carotids, femoral, brachial)

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32
Q

What are the 2 heart sounds?

A

I - closure of atria-ventricular valves
II - closure of semi-lunar valves

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33
Q

It is unusual to have more than 2 heart sounds, what can it indicate?

A

Indicates sign of very high cardiac output state

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34
Q

What is a heart murmur?

A

Turbulent blood flow

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35
Q

When does turbulence occur?

A

Turbulence occurs when a fluid is passing through an aperture at a too high velocity, causing a murmur (whoosh) sound.

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36
Q

When and where can a murmur occur?

A

Systole or diastole
Systole occurs after you hear the first heart sound (lub)
Diastole occurs after the second heart sound (dub)
It is heard on the precordium. How loud should be considered.

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37
Q

What is a heave and what is it a sign of?

A

Chest wall pushed during systole
A sign of ventricular hypertrophy, or aortic/pulmonary stenosis potentially

38
Q

How do you grade murmurs via the Levine system? (POTENTIAL EXAM MCQ QUESTION)

A

I - faint, expert ears, prolonged auscultation
II - faint, but immediately audible
III - loud, not palpable
IV - loud, associated with thril
V - audible stethoscope barely in contact
VI - audible stethoscope not in contact

39
Q

What is coronary artery disease the same as?

A

Coronary artery disease = ischaemic heart disease

40
Q

Anatomy refresher, what arteries supply the myocardium with blood? (PG536 IMG)

A

Coronary artery arises from the aorta.
Left anterior descending artery = most dominant artery, supplying around 60-90% of the myocardium with blood
Some of these anastomose, so blood supply overlaps, so blocking is very problematic.

41
Q

What is the problem in coronary artery/ischaemic heart disease?

A

Not enough blood supply to the heart. So an imbalance of myocardial oxygen supply and demand causing a buildup of waste metabolites.

42
Q

What is the pathophysiology of coronary artery disease?

A

Atherosclerosis in coronary arteries (deposition of fatty plaques)

43
Q

When does coronary perfusion occur?

A

Coronary perfusion occurs during diastole only, about 2/3’s of the time

44
Q

What does reducing the radius size of the arteries do?

A

Reducing radius increases resistance by a factor of 4
>50% cross-sectional stenosis (narrowing) = flow limiting

45
Q

When do patients notice the flow limiting lesion?

A

When heart rate accelerates, you reduce diastolic time. So when patients HR increases, they will notice the flow limiting lesion. Eg limits blood flow during exercise (when you need higher blood flow).

46
Q

What can stenosis and occlusion lead to?

A

Stenosis leads to angina
Occlusion leads to heart attack (myocardial infarction)

47
Q

What are the symptoms of coronary artery disease?

A

Chest pain (angina pectoris)
Shortness of breath (dyspnoea)

48
Q

What is the aim of treatment for coronary artery/ischaemic heart disease?

A

To improve blood supply to heart and decrease risk of myocardial infarction

49
Q

What are all of the different medications that could be used for coronary artery/ischaemic heart disease?

A

Beta blockers, Ca antagonists, nitrates, nicorandil
Aspirin, clopidogrel, statins, ACE inhibitors

50
Q

How is IHD prevention?

A

Diet (low fat)
Exercise
Weight loss
Smoking cessation
Glycaemic control
Cholesterol control
Hypertensive control
Anti-platelet agents - aspirin

51
Q

What can be given for symptomatic relief of angina?

A

Nitrates eg GTN, isosorbide mononitrate etc
Beta blockers
Nicorandil
Ivabradine
Ranolazine

52
Q

How do nitrates like GTN or isosorbide mononitrate help symptoms of angina?

A

It vasodilates arteries, helping improve flow
Selective for collateral vessels
Also reduces afterload, so resistance and work decreases, thus reduced energy demand

53
Q

How do beta blockers help symptoms of angina?

A

They slow the heart down
Increase duration of diastole, so increases coronary perfusion time and thus supply of oxygen
Decreases contractility and thus energy demand

54
Q

Give an example of a beta blocker?

A

Bisoprolol (ends in -olol)

55
Q

What drugs have the same effect as beta blockers on the heart?

A

Rate limiting calcium blockers eg verapamil, diltiazem
(amlodipine is not rate limiting so does not have anti-angina effects)

56
Q

What does nicorandil do?

A

Coronary vasodilator by hyperpolarisation of endothelium, so myocardium has less force when it contracts

57
Q

What does ivabradine and Ranolazine do?

A

Ivabradine - slows heart rate - direct action on the SAN
Ranolazine - decreases peak intracellular Ca2+ thus reduces contractility

58
Q

What medical treatments can be given in CAD/IHD to prevent MI?

A

Antiplatelet agents
Cholesterol lowering

59
Q

How do anti-platelet agents reduce risk of MI?

A

Reduce platelet binding to exposed tissue factor and thus reduce subsequent aggregation. Thus reduces proliferation of the thrombus.

60
Q

What Antiplatelet agents are there and what do they do?

A

Aspirin - COX inhibitor thus reduces TXA2 production
Clopidogrel - competitively inhibits ADP binding to P2Y12 receptors on platelets which is required for the activation on GPIIa/IIIb complex for platelet aggregation
Prasugrel - same mechanism as clopidogrel but quicker onset and more reliable
Ticagrelor - same mechanism but non-competitive, reversible inhibitor

61
Q

When should you pause aspirin mono therapy?

A

5 days pre-procedure

62
Q

When should you pause clopidogrel/prasugrel/ticagrelor?

A

D/C cardiologist reason why and ask if it is safe to pause

63
Q

When is it unsafe to stop agents prior to a surgery?

A

Unsafe to stop agents prior to 6 weeks after stent surgery

64
Q

What cholesterol lowering agents are there?

A

Statins (end in -statin)
Ezetimibe

65
Q

What do statins do?

A

Competitive reversible inhibit HMG-CoA reductase by mimicking its substrate
Rate-limiting step in cholesterol synthesis
This prompts hepatic reuptake of LDLs and VLDLs (bad cholesterol) (which leads to plaques in arteries being unstable, likely to rupture and therefore cause distal occlusion through thrombus formation).
(More effective than ezetimibe)
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, an enzyme involved in cholesterol synthesis, especially in the liver

66
Q

What coronary surgeries can be performed?

A

Coronary artery bypass grafting (CABG)
Valve operations

67
Q

What is percutaneous coronary intervention (PCI)?

A

Performed by cardiologist in the catheter lab
Angiogram using intravenous contrast to assess coronary anatomy
Some lesions are suitable for stenting

68
Q

Which lesions are suitable for stenting?

A

Discrete lesions are stentable
Long diffuse ones are not

69
Q

What is a coronary artery bypass graft?

A

The surgical management of coronary artery disease. Indicated for symptomatic relief and prognosis (survival advantage in stable angina)
Sternotomy to find the heart
Plum veins and arteries into the heart past the blockages and connect to the heart

70
Q

What are the benefits of PCI?

A

Survival advantage during STEMI
Symptomatic relief of stable angina (no survival advantage in stable angina)

71
Q

What are the indications for coronary surgery?

A

Relief of symptoms - most can stop anti-angina meds after
Improvement of prognosis - reduced risk of MI

72
Q

What is the emergency treatment of MI? - EXAM Q

A

Oxygen (15L non re-breathable)
Nitrates - sublingual GTN spray
Antiplatelet agents - aspirin 300mg (AND clopidogrel 300mg or prasugrel 75mg or ticagrelor 90mg)
Analgesics (preferable opiates eg morphine or fentanyl - effective and reduced after load)
Ambulance

73
Q

What problems can you have with valves?

A

Stenosis = too tight, valve resists blood flow
Regurgitation = too leaky, valve allows back flow
Both increase myocardial work and cause ventricles to remodel

74
Q

What are some causes of valvular heart disease?

A

Myxomatous degeneration
Endocarditis
Rheumatic fever
Rarities eg carcinoid disease

75
Q

What is Laplace’s law?

A

T = (P x r)/2h
Tension inside a wall depends on the pressure inside the cavity, radius of cavity and thickness of the wall
Thus if increasing pressure, you increase tension. The heart responds by increasing wall thickness, making it stiffer and less pumping etc.

76
Q

What happens if you have a regurgitant lesion (according to Laplace’s law)?

A

If you have a regurgitation lesion, allowing lots of blood flow back into it, this will create an increased radius, thus increased tension and thus increased wall thickness. Hence unuseful heart remodelling.

77
Q

Critical aortic stenosis is the most common form of valvular disease. What is it?

A

Narrowing of the aortic valve (between the left ventricle and aorta)

78
Q

Why should you not give in critical aortic stenosis?

A

Sedatives (eg midazolam) - these reduce SVR (systemic vascular resistance). MAP = CO X SVR,
If CO is fixed, decreased SVR = decreased MAP —> decreased coronary blood flow —> myocardial ischaemia —> decreased CO

79
Q

Mechanical solutions are more effective for managing valvular heart disease but what medicines can reduce the symptoms of heart failure (eg dyspnoea, oedema)?

A

Diuretics
ACE inhibitors - reduces afterload, reduces maladaptive cardiac remodelling
Specific Tx directed at cause - eg antibiotics for endocarditis or somatostatin for carcinoid disease (rarer)

80
Q

What surgical management options are there for valvular disease?

A

Valve repair
Valve replacement (tissue or mechanical)

81
Q

What do mechanical prosthesis require?

A

Anticoagulation

82
Q

Why is Anticoagulation needed in patients with mechanical prosthesis?

A

To prevent thrombus formation
This occludes the valve and if embolises will cause stroke

83
Q

What is the target INR with warfarin for aortic and mitral?

A

Aortic INR target 2.5 (not too bleedy)
Mitral INR target 3.5 (very bleedy)

84
Q

What’s the difference between tissue valve replacement and mechanical valve replacement?

A

Tissue valve: low risk thrombosis, no Anticoagulation. Limited durability, increased deterioration eg in pregnancy
Mechanical valve: indefinite lifespan, excellent haemodynamics. Lifelong Anticoagulation, audible click.

85
Q

What are the complications of cardiac surgery?

A

Death
Myocardial infarction
Stroke
Bleeding
Infection - systemic sepsis; wound, mediastinitis
Respiratory failure eg pneumonia, ARDS
Renal failure
Abdominal - ischaemic bowel, GI bleed

86
Q

What is infective endocarditis? EXAM POTENTIAL

A

An infection of the endothelial surface of the heart by a microorganism due to bacteraemia

87
Q

Why does infective endocarditis have a high morbidity and mortality?

A

High mortality as limited ability to get rid of all of the abscess contents out without getting rid of a lot of the heart

88
Q

What can cause transient bacteraemia?

A

Dental work - any oral procedure (even brushing) can lead to transient bacteraemia, more invasive procedures lead to increased bacterial load
IV drug abuse
Other invasive procedures - gastroenterological, genitourinary, ENT

89
Q

What are some common causative organisms for bacteraemia?

A

Streptococcus viridans group
Staphylococcus aureus

90
Q

According to NICE, which patients are at risk of endocarditis?

A

Valvular heart disease
Valve replacement
Structural congenital heart disease
Previous endocarditis
Hypertrophic cardiomyopathy

91
Q

What are the current NICE guidelines on antibiotic prophylaxis against infective endocarditis?

A

Antibiotic prophylaxis not recommended routinely for any patients undergoing dental procedures

Human Diseases (75 decks)

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