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Bateman - Phase 2a COPY > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

What is atherosclerosis?

A

Atherosclerosis is a disease in which plaque builds up inside your arteries.

Principal cause of heart attack, stroke and gangrene of the extremities.

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2
Q

What is the main problem of atherosclerosis?

A

Plaque ruptures leading to thrombus formation and ultimately death.

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3
Q

What are the risk factors for atherosclerosis?

A

Age.

Tobacco smoking.

High Serum Cholesterol.

Obesity.

Diabetes.

Hypertension.

Family History.

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4
Q

What is the distribution of atherosclerotic plaques? How can the distribution be altered?

A

Found within peripheral and coronary arteries. Focal distribution along the artery length.

Distribution may be altered by haemodynamic factors.

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5
Q

What do changes in flow/turbulence cause the artery to do?

A

Adjust its wall thickness - develop neoihtima. Also alter gene expression.

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6
Q

What is neoihtima?

A

Neointimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space.

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7
Q

What does an atherosclerotic plaque a complex lesion consist of?

A

Lipid.

Necrotic core.

Connective tissue.

Fibrous cap.

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8
Q

What will eventually happen when the plaque gets bigger and bigger?

A

Occlude the vessel resulting in angina or will rupture.

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9
Q

When is inflammation good?

A

When its protecting against:

Pathogens.

Parasites.

Tumours.

Wound healing.

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10
Q

When is inflammation bad?

A

Myocardial repercussion injury.

Atherosclerosis.

Ischaemic heart disease.

Rheumatoid arthritis.

Asthma.

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11
Q

What ignites inflammation in the arterial wall during atherosclerosis?

A

LDLs - they can pass in and out of the arterial wall in excess, accumulates in arterial wall, undergoes oxidation and glycation.

and

Endothelial dysfunction - signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.

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12
Q

What happens when injury occurs to the endothelial cell?

A

Chemoattractants are released from endothelium and send signals to leukocytes.

A concentration gradient is produced.

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13
Q

What are some inflammatory cytokines found in plaques?

A

IL-1.

IL-6.

IL-8.

IFN-gamma.

TGF-Beta.

MCP-1 (C reactive protein).

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14
Q

What is involved with leukocyte recruitment to vessel walls?

A

Selectins.

Capture. Rolling. Slow rolling.

Integrins and chemoattractants

Frim adhesion. Transmigration.

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15
Q

What is stage 1 of atherosclerosis? What does it consist of?

A

Fatty streaks.

Appear at very early age.

Consist of aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall.

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16
Q

What is stage 2 of atherosclerosis? What does it consist of?

A

Intermediate lesions.

Consists of same as stage 1 plus:

Vascular smooth muscle cells.

Adhesion and aggregation of platelets to vessel wall.

Isolated pools of extracellular lipid.

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17
Q

What is stage 3 of atherosclerosis?

A

Fibrous plaques or advanced lesions.
Impedes blood flow.
Prone to rupture.

Covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris.

May be calcified.

Contains: Smooth muscles cells, macrophages and foam cells and T lymphocytes.

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18
Q

What is stage 4 of atherosclerosis?

A

Plaques rupture.
Plaques constantly growing and receding.
Fibrous cap has to be resorbed and redeposited in order to be maintained.

If balance is shifted in favour of inflammatory conditions (increased enzyme activity), the cap becomes weak and the plaque ruptures.

Basement membrane, collagen, and necrotic tissue exposure as well as haemorrhage of vessels within the plaque.

Thrombus (clot) formation and vessel occlusion.

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19
Q

What are the basic steps of atherosclerosis?

A

Fatty steaks.

Intermediate lesions.

Fibrous plaques or Advanced lesions.

Plaques rupture.

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20
Q

What is the treatment of atherosclerosis?

A

Percutaneous coronary intervention. (stents)

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21
Q

What are the epicardial vessels?

A

Left and right coronary artery, they lie on the surface of the heart.

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22
Q

What are two drugs used for coronary artery disease drug eluting stents?

A

Taxus Brevifolia (Taxol)

Streptomyces hygroscopicus (Sirolimus)

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23
Q

What is angina? why does it happen?

A

A SYMPTOM which occurs as a consequence of restricted coronary blood flow. Mismatch between oxygen demand and oxygen supply.

Usually shown by CHEST PAIN

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24
Q

What is a SCAD?

A

A Spontaneous Coronary Artery Dissection

Tear forms in a blood vessel in the heart.

As blood flow is slowed or blocked entirely

Result can be a heart attack, heart rhythm abnormalities, or sudden death.

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25
Q

What is ACS?

A

Acute Coronary Syndrome.

Syndrome (set of signs and symptoms)

Decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.

Chest pain, often radiating to the left shoulder or angle of the jaw, crushing, central and associated with nausea and sweating.

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26
Q

What does UA/NSTEMI stand for?

A

Unstable angina, non ST elevation myocardial infarction

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27
Q

What does myogenic control of blood flow allow?

A

Ensures that blood flow remains constant in a physiological range of blood pressure. Beyond this range, myogenic control fails and flow is affected.

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28
Q

How does an oxygen supply demand mismatch occur?

A

Impairment of blood flow by proximal arterial stenosis.

Increased distal resistance eg left ventricular hypertrophy.

Reduced oxygen-carrying capacity of blood e.g. anaemia.

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29
Q

What does the diameter of the vessel have to fall below before symptoms occur?

A

75%.

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30
Q

Electro-hydraulic analogy. What is a healthy system like at rest with the epicardial and microvasculature?

A

The resistance of the epicardial artery is negligible and so the flow through the system is determined by the resistance (tone) of the microvascular vessels.

Total flow around 3 ml/s.

LOW EPICARDIAL MODERATE MICROVASCULATURE.

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31
Q

Electro-hydraulic analogy. What happens in a healthy system when exercising?

A

Under exercise conditions more flow is needed to metabolic demand. The microvascular resistance falls so the flow can increase.

Total flow around 15 ml/s.

LOW ON BOTH.

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32
Q

Electro-Hydraulic analogy. What happens in a diseased person at rest?

A

Epicardial disease causes the resistance of the epicardial vessel to increase.

To compensate, the microvascular resistance reduces in order to maintain flow at 3 ml/s.

HIGH EPICARDIAL LOWER

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33
Q

Electro-hydraulic analogy. What happens in a diseased person during exercise?

A

Epicardial resistance is high due to the stenosis. During exercise the microvascular resistance falls to try and increase flow.

However, there comes a point where minimising microvascular resistance is maxed out and can fall no more. At this point, flow cannot meet metabolic demand.

The myocardium becomes ischaemic and pain is typically experienced. The only way to reverse this is to rest, thus reducing the demand for flow.

HIGH EPICARDIAL NOT LOW ENOUGH MICROVASCULAR

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34
Q

What are some other anginas apart from SCAD and ACS?

A

Prinzmetal’s angina (coronary spasm).

Microvascular angina (Syndrome X).

Crescendo angina and unstable angina ACS.

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35
Q

What are some risk factors for IHD?

A

Non-modifiable

Gender.
Family history.
Personal history.
Age.

MODIFIABLE.

Smoking.
Diabetes
Hypertension.
Hypercholesterolaemia.
Sedentary lifestyle.

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36
Q

What are the different types of angina?

A

Stable angina: induced by effort, relieved by rest.

Unstable angina: angina of increasing frequency or severity; occurs on minimal exertion or at rest; associated with increased risk of MI.

Decubitus angina: precipitated by lying flat.

Variant (Prinzmetal’s) angina: caused by coronary artery spasm.

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37
Q

What are the causes of angina?

A

Mostly atheroma.

Rarely:
anaemia,
AS; tachyarrhythmias; HCM; arteritis/ small vessel disease.

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38
Q

What are the symptoms of angina?

A

Chest pain/discomfort.

Heavy, central, tight, radiation to arms, jaw, neck.

Precipitated by exertion.

Relieved by rest /sl GTN.

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39
Q

What are the differential diagnoses for angina?

A

Pericarditis/ myocarditis.

Pulmonary embolism.

Chest infection.

Dissection of the aorta.

Gastro-esophageal reflux.

Musculo-skeletal.

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40
Q

What are the basic investigations for stable IHD (angina)?

A

12 lead ECG.
Often normal - there are no direct markers of angina.
Signs of IHD - Q waves, T waves inversion, BBB.

Echo.
Normal - no direct markers of angina.
Signs of
previous infarcts.
Q waves, T-wave inversion.
Alternative diagnoses.

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41
Q

What are the management options for angina pectoralis?

A

Modify risk factors: stop smoking, encourage exercise, weight loss, control hypertension, diabetes.

Statin. (atorvastatin (Lipitor), (simvastatin (Zocor)).

Aspirin.

Beta-blockers, eg atenolol.

Nitrates: for symptoms, GTN spray or sublingual tabs.

Prophylaxis: oral nitrate, eg isosorbide mononitrate Alternatives: adhesive nitrate skin patches or buccal pills.

Long-acting calcium antagonists: amlodipine.They are particularly useful if there is a contraindication to beta-blockers.

K + channel activator, eg nicorandil

Others: ivabradine inhibits the pacemaker (‘funny’) current in the SA node and thus reduces heart rate. Useful in those who cannot take a beta-blocker, having similar ef- ficacy. Trimetazidine inhibits fatty acid oxidation, leading the myocardium to use glucose, which is more efficient. Ranolazine inhibits the late Na+ current.

Unstable angina requires admission and urgent treatment: emergencies,

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42
Q

What are some diagnostic investigations for stable IHD (angina)?

A

Anatomical

CT angiography (NI)
Invasive angiography (I)

Physiological (stress and rest)

Exercise stress treadmill (NI)
Stress echo (NI)
SPECT (nuclear perfusion) (NI)
Perfusion (stress) MRI (NI)

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43
Q

What is the pre-test probability of CAD? What is it used for?

A

Used to assess for the presence of coronary stenoses.

Determines options if low, intermediate or high probability.

Low = Other cause?

Intermediate = Testing

High = Offer treatment

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44
Q

What is the treadmill test?

A

Induce ischaemia while walking uphill, incrementally fast

Look for ST segment depression

Detects a ‘late stage’ of ischaemia

Many patients unsuitable
Can’t walk
Very unfit
BBB
Young females.

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45
Q

What does the CT angiogram show?

A

High NPV.

Low PPV.

Ideal for excluding CAD in younger, low risk individuals.

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46
Q

How does an invasive angiogram work?

A

Catheter inserted into an artery in the groin up to the aorta, dye is injected and x-rays are taken of it.

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47
Q

How does a Single Photon Emission Computed Tomography (SPECT) work?

A

Radioactive tracer taken up by tissues of heart.

Ultrasound of the heart taken under exercise.

1st scan - under stress.

2nd scan - bring back to rest.

Fixed defect = scar. Reversible defect = ischaemia.

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48
Q

What is primary prevention of IHD?

A

Reducing the risk of CAD and complications.

Risk factor modification.

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49
Q

What is secondary prevention of IHD?

A

Risk factor modification.

Symptomatic therapy vs prognostic therapy.

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50
Q

What is the SCORE system? What are the primary prevention options for stable IHD?

A

Systemic coronary risk estimation tool.

Hypertension - Antihypertensives

Hypercholesterolaemia - Statins + lipid modulating therapies

T2DM - Diabetic therapy

Smoking - Smoking cessation

Diet - General advice

Exercise - Get plenty

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51
Q

What are the secondary prevention options for stable IHD?

A

Lifestyle changes
risk factor and behaviour modification
akin to primary prevention

Pharmacological
to reduce cardiovascular events (e.g. aspirin, statins)
to reduce symptoms (e.g. nitrates, CCBs, KCBs)

Interventional (PCI and sometimes surgery)
to reduce events (if large (≥10%) amount of ischaemic myocardium)
to reduce symptoms.

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52
Q

What pharmacological options are available for stable IHD?

A

Beta blockers.

Nitrates.

Calcium channel antagonists.

Antiplatelets.

Statins.

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53
Q

What are some examples of beta blockers and what do they do?

A

Bisoprolol and atenolol.

Antagonise sympathetic nervous activation.
Reduce heart rate (-ve chronotrope).
Reduce contractility (-ve inotrope).

Therefore reduce work of heart and oxygen demand.]

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54
Q

What are the side effects of beta blockers?

A

Tiredness, nightmares.

Erectile dysfunction.

Bradycardia.

Cold hands and feet.

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55
Q

What are some contra-indications to beta blockers?

A

Excess bradycardia.

Severe heart block.

Severe bronchospasm; asthma.

Prinzmetal’s angina.

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56
Q

How do nitrates work?

A

Primarily venodilators

Dilate systemic veins (reduce venous return to R heart)

Reduce preload on the heart

Therefore (via Frank-Starling mechanism) reduce work of heart and O2 demand

(also dilate coronary arteries – antagonise spasm).

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57
Q

How do calcium channel antagonists work?

A

Primarily arterodilators

Dilate systemic arteries (↓BP)

Reduce afterload on the heart

↓ energy required to produce same cardiac output

Therefore reduce work of heart and O2 demand

(also dilate coronary arteries – antagonise spasm)

(non-dihydropyridines are also negatively inotropic).

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58
Q

What are some examples of calcium channel antagonists?

A

Nicorandil (2nd line antianginal):
Mixed veno- and artero-dilatory properties

Ivabridine (2nd line antianginal):
’Funny’ sodium channel to slow pacemaker currents
Only useful in sinus rhythm
Slow sinus rhythm (negative chronotrope).

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59
Q

How do antiplatelets work?

A

Reduce events

Aspirin - salicylate (Salix = willow tree)

Cyclo-oxygenase inhibitor

↓ prostaglandin synthesis, incl. thromboxane

↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic

Caution! – gastric ulceration.

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60
Q

How do statins work?

A

Reduce events

Reduce LDL-cholesterol

Anti-atherosclerotic but…

…other mechanisms of action proposed

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61
Q

What is CABG?

A

Coronary artery bypass surgery.

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62
Q

What are the pros and cons of PCI?

A

PROS Less invasive Convenient Repeatable Acceptable CONS Risk stent thrombosis Risk restenosis Can’t deal with complex disease Dual antiplatelet therapy

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63
Q

What are the pros and cons of CABG?

A

PROS Prognosis Deals with complex disease CONS Invasive Risk of stroke, bleeding Can’t do if frail, comorbid One time treatment Length of stay Time for recovery

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64
Q

What does acute coronary syndromes include?

A

Lots of cardiac conditions including unstable angina to varying degrees of evolving myocardial infarction.

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65
Q

What is the clinical classification of unstable angina?

A

Cardiac chest pain at rest. Cardiac chest pain with crescendo pattern. New onset angina.

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66
Q

What are the different acute myocardial infarctions and how are they diagnosed?

A

ST-elevation MI can usually be diagnosed on ECG at presentation

Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

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67
Q

How can normal myocardial infarctions be diagnosed?

A

May also be defined retrospectively as non-Q wave or Q-wave MI on the basis of whether new pathological Q waves develop on the ECG as a result of it

ST elevation MI and MI associated with LBBB are associated with larger infarcts unless effectively treated (and therefore more likely to lead to pathological Q wave formation, heart failure or death).

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68
Q

What can an MI also be defined by retrospectively?

A
  • May also be defined retrospectively as non-Q wave or Q-wave MI on the basis of whether new pathological Q waves develop on the ECG as a result of it
  • ST elevation MI and MI associated with LBBB are associated with larger infarcts unless effectively treated (and therefore more likely to lead to pathological Q wave formation, heart failure or death)
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69
Q

What puts people at a higher risk of a MI?

A

Higher risk associated with

higher age,

diabetes,

renal failure,

left ventricular systolic dysfunction (elevated NT-proBNP level) and

other risk factors

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70
Q

What usually happens in a myocardial infarction?

A

Usually causes permanent heart muscle damage although this may not be detectable in small MIs.

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71
Q

What are the symptoms of a myocardial infarction?

A

Cardiac chest pain

  • unremitting
  • usually severe but may be mild or absent
  • occurs at rest
  • associated with sweating, breathlessness, nausea and/or vomiting
  • one third occur in bed at night.
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72
Q

What is the initial management for a MI?

A
  • Get in to hospital quickly – 999 call
  • Paramedics – if ST elevation, contact primary PCI centre for transfer
  • Take aspirin immediately
  • Pain relief
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73
Q

What is the hospital management of a MI?

A
  • Make diagnosis
  • Bed rest
  • Oxygen therapy if hypoxic
  • Pain relief – narcotics/ nitrates
  • Aspirin +/- P2Y12 inhibitor
  • Consider beta-blocker
  • Consider other antianginal therapy
  • Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy
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74
Q

What are the main causes of ACS?

A

Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases. Uncommon causes include coronary vasospasm without plaque rupture, drug abuse (amphetamines, cocaine), dissection of the coronary artery related to defects of the vessel connective tissue, and thoracic aortic dissection .

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75
Q

Why is troponin important in monitoring heart disease?

A

Protein complex regulates actin:myosin contraction

Highly sensitive marker for cardiac muscle injury

Not specific for acute coronary syndrome

May not represent permanent muscle damage

Positive also in: gram negative sepsis pulmonary embolism myocarditis heart failure arrhythmias cytotoxic drug.

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76
Q

What factors are contained in the endothelial wall?

A

VWF and collagen.

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77
Q

What factors does initial adhesion of a platelet require?

A

GPIB/VWF.

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78
Q

What factors does rolling of a platelet require?

A

GPIb/VWF alpha2beta1/collagen.

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79
Q

What factors does stable adhesion activation/aggregation require?

A

GPVI and GPIIb/IIIa.

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80
Q

What does collagen act on? what does this do? What inhibits this?

A

GPVI which activators thromboxane to cause more platelet activation.

Aspirin inhibits this.

COX-1 is being inhibited.

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81
Q

What does the platelet activation produce? What does each aspect do?

A

Thrombin generation to aid with coagulation.

Alpha granule release to contribute to coagulation and inflammation.

Dense grail release to contribute to more platelet activation.

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82
Q

What does Fibrin do?

A

Holds platelets together.

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83
Q

How does the fibrinolytic system work?

A

tPA released from endothelial cells which causes plasminogen to go to plasmin.

Plasmin then causes fibrin to go to FDP.

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84
Q

What is the role of P2Y12?

A

Causes amplification of the clot forming system.

More platelet activation.

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85
Q

What are some P2Y12 antagonists?

A

Clopidogrel.

ORAL Prasugrel.

ORAL Ticagrelor.

ORAL Cangrelor.

INTRAVENOUS

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86
Q

What is a risk of P2Y12 antagonists?

A

Increased bleeding.

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87
Q

What do anticoagulants do? What are some examples?

A

Target formation and/or activity of thrombin.

Inhibit both fibrin formation and platelet activation.

Heparin.

Fondaparinux.

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88
Q

What are GPIIb/IIIa antagonists?

A

Stop fibrinogen and aggregation.

Only intravenous drugs available.

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89
Q

What are the signs and symptoms of DVT?

A

Symptoms and signs non- specific, clinical diagnosis unreliable.

Symptoms:

pain, swelling

Signs:

tenderness, swelling, warmth, discolouration.

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90
Q

What are some tests for DVT?

A

D-dimer:

Normal excludes diagnosis positive does not confirm diagnosis

Ultrasound compression test proximal veins

(venogram for calf, recurrence, uncertain).

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91
Q

What are the treatments for DVT?

A

LMW Heparin

Oral warfarin

Compression stockings

Treat/ seek underlying cause: malignancy, thrombophilia

Spontaneous DVT more likely to recur (10% per year) than provoked.

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92
Q

What are the risk factors for DVT?

A

Surgery, immobility, leg fracture/ POP

OC pill, HRT, Pregnancy

Long haul flights/ travel (rare)

Inherited thrombophilia- genetic predisposition; 5% population, familial.

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93
Q

What are the prevention methods for DVT?

A

Mechanical- hydration and early mobilisation, Compression stockings, Foot pumps

Chemical- LMW Heparin.

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94
Q

What are the signs and symptoms of a pulmonary embolism?

A

Symptoms: breathlessness, pleuritic chest pain, may have signs/ symptoms of DVT, may have risk factors, no other diagnosis more likely

Signs: tachycardia, tachypnoea, pleural rub, those of precipitating cause, none of alternative diagnosis.

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95
Q

What are the differential diagnosis for SOB and chest pain?

A

Pulmonary embolism

  • Differential diagnosis of chest pain and sob
  • Consider also musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro causes
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96
Q

What are the pulmonary embolism initial investigations? Further investigations?

A

INITIAL

CXR usually normal

ECG sinus tachy, (QI,SI,TIII)

Blood gases: type 1 resp failure, decreased O2 and CO2.

FURTHER

D-dimer: normal excludes diagnosis

Ventilation/ Perfusion scan: mismatch defects

CTPA spiral CT with contrast, visualise major segmental thrombi

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97
Q

What is the treatment for pulmonary embolism?

A

As for DVT

Ensure normal Hb, platlets, renal function, baseline clotting

LMW Heparin s/c od weight adjusted 5/7 Oral warfarin INR

DOAC

Treat cause if possible

If cannot anti-coagulate, consider IVC filter.

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98
Q

What is the prevention of pulmonary embolism?

A

Same as for DVT

Early mobilisation and hydration

Mechanical

Chemical: LMW Heparin s/c od.

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99
Q

What is a Thrombosis?

A

Blood coagulation inside a vessel.

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100
Q

Where can thrombosis occur?

A

arterial circulation: high pressure: platelet rich

venous circulation: low pressure: fibrin rich

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101
Q

What is a thrombosis called when it happens in different parts of the body?

A

Coronary circulation = myocardial infarction

Cerebral circularion = CVA/ stroke

Peripheral circulation = peripheral vascular disease: claudication, rest pain, gangrene

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102
Q

What are the risk factors for atherosclerosis?

A

Smoking

Hypertension

Diabetes

Hyperlipidaemia

Obesity / sedentary lifestlye

Stress / type A personality.

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103
Q

What investigations should you do for each thrombosis in the different part of the body?

A

Myocardial infarction: diagnosis History, ECG, cardiac enzymes

CVA: history and examination, CT scan/ MRI scan

Peripheral vascular disease: history and examination, ultrasound, angiogram.

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104
Q

How do you treat a myocardial infarction?

A

Myocardial infarction:

Aspirin

LMWH or Fondraparinux

Thrombolytic therapy: streptokinase tissue plasminogen activator

Aspirin inhibits platelet function

TPA generates plasmin, degrades fibrin

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105
Q

How do you treat a stroke?

A

Stroke

Aspirin or clopidogrel, prasugrel, tiglacor: anti-platelet

TPA (brain attack, narrow window)

Treat risk factors.

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106
Q

What are the different types of venous thrombosis?

A

Deep venous thrombosis =

swollen, warm, tender leg

Pulmonary embolus =

pleuritic chest pain, breathlessness, cyanosis, death.

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107
Q

What investigations would you do for each venous thrombosis?

A

DVT compression ultrasound
+/- doppler

Pulmonary embolus: CT scan
CT pulmonary angiogram

V/Q or perfusion scan

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108
Q

What are the circumstantial causes of a venous thrombosis?

A

Causes: circumstantial

Surgery

Immobilisation

Oestrogens: OC, HRT

Malignancy

Long haul flights.

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109
Q

What are the genetic causes of a venous thrombosis?

A

Causes: genetic

Factor V Leiden (5%)

PT20210A (3%)

Antithrombin deficiency

Protein C deficiency

Protein S deficiency

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110
Q

What are the acquired causes of a venous thrombosis?

A

Causes: acquired

Anti-phospholipid syndrome

Lupus anticoagulant

Hyperhomocysteinaemia

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111
Q

What is the treatment for venous thrombosis?

A

Initial

Low molecular weight heparin, s/c od weight adjusted dose

Then oral warfarin for 3-6 months

Or DOAC for 3-6 months, e.g. Rivaroxaban 15mg bd initially then 20mg od.

DOAC = Direct oral anti-coagulants

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112
Q

What is the prevention for venous thrombosis?

A

Prevention

Thromboprophylaxsis

od, s/c, LMWH

TED stockings

early mobilisation and good hydration.

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113
Q

What is Heparin and what does it do?

A

Glycoaminoglycan

Binds to antithrombin and increases its activity

Indirect thrombin inhibitor

Given by continuous infusion.

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114
Q

What is aspirin and what does it do?

A

Inhibits cyclo-oxygenase irreversibly

Act for lifetime of platelet, 7-10 days

Inhibits thromboxane formation and hence platelet aggregation

Used in arterial thrombosis

Clopidogrel similar, but inhibits ADP induced platelet aggregation

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115
Q

What is warfarin and what does it do?

A

Orally active

Prevents synthesis of active factors II, VII, IX and X

Antagonist of vitamin K

Long half life (36 hours)

Prolongs the prothrombin time.

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116
Q

What do genes do?

A

Make proteins.

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117
Q

What does cardiomyopathy refer to?

A

primary heart muscle disease – often genetic.

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118
Q

What is Hypertrophic cardiomyopathy (HCM) caused by? How many people does it affect?

A

Sarcomeric protein gene mutations. 1 in 500 people.

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119
Q

What happens in HCM?

A

Unexplained primary cardiac hypertrophy.

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120
Q

What are the symptoms of HCM?

A

Angina. Dyspnoea. Palpitations. Dizzy spells or syncope. Left Ventricular Outflow Tract Obstruction maybe.

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121
Q

What is Dilated cardiomyopathy (DCM) often caused by?

A

Cytoskeletal gene mutations.

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122
Q

What does DCM usually present with? What are the symptoms?

A

Heart failure symptoms. LV/RV or 4 chamber dilatation and dysfunction.

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123
Q

What is Arrhythmogenic cardiomyopathy (ARVC/ALVC) caused by?

A

Desmosome gene mutations.

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124
Q

What is the main feature of arrhythmogenic cardiomyopathy?

A

Arrhythmia.

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125
Q

What do all cardiopathies carry?

A

An arrhythmic risk.

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126
Q

What is Inherited arrhythmia (channelopathy) caused by?

A

Ion channel protein gene mutations.

127
Q

Which ions are involved with channelopathy?

A

potassium, sodium or calcium channel.

128
Q

What do channelopathies include?

A

Long QT, short QT, Brugada and CPVT.

129
Q

What do channelopathies normally present with and what do they have that is normal?

A

Recurrent syncope and have a structurally normal heart.

130
Q

What is sudden cardiac death in young people normally due to? What disease is it most likely to be?

A

An inherited condition. Cardiomyopathy or ion channelpathy.

131
Q

What does sudden arrhythmic death syndrome (SADS) usually refer to?

A

Normal heart/arrhythmia.

132
Q

What is familial hypercholesterolaemia (FH)?

A

Inherited abnormality of cholesterol metabolism.

133
Q

What does FH lead to?

A

Serious premature coronary other vascular disease.

134
Q

What are common problems to be inherited?

A

Aortic aneurysm or dissection.

135
Q

What aortavascular syndromes are there?

A

Marfan, Loeys-Dietz, vascular Ehler Danlos (EDS).

136
Q

What are ICCs inheritance?

A

Dominantly with a 50% risk.

137
Q

What does each individual need?

A

An different risk check, genetic testing which is available for many of these diseases.

138
Q

How many layers is the pericardium? What is the structure?

A

Two. Visceral single cell layer adherent to epicardium Fibrous parietal layer 2mm thick Acellular collagen and elastin fibres 50ml of serous fluid.

139
Q

What is contained within the pericardium? What is outside?

A

Great vessels lie within the pericardium Two layers are continuous Left atrium is mainly outside the pericardium Parietal layer has fibrous attachments to fix the heart in the thorax.

140
Q

Why is the pericardium important? What is important about the small reserve volume?

A

Restrains the filling volume of the heart. If the volume is exceeded the pressure is translated to the cardiac chambers.

141
Q

What is cardiac tamponade?

A

Fluid builds up in the pericardium and results in compression of the heart.

142
Q

What does chronic pericardial effusion have that is unique?

A

Pericardium slowly adapts to the increasing fluid and therefore reduces the effect on diastolic filling of the chambers.

143
Q

What is acute pericarditis?

A

Inflammatory pericardial syndrome with or without effusion.

144
Q

How can acute pericarditis be diagnosed?

A

Chest pain. Friction rub. ECG changes. Pericardial effusion.

145
Q

What are the viral (common) causes of acute pericarditis?

A

Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis).

146
Q

What are the bacterial causes of acute pericarditis?

A

Mycobacterium tuberculosis (other bacteria rare).

147
Q

What are the non-infectious ways to get acute pericarditis? Autoimmune (common)?

A

Autoimmune (common): Sjögren syndrome, rheumatoid arthritis, scleroderma, systemic vasculitides.

148
Q

What are the non-infectious ways to get acute pericarditis? Neoplastic?

A

Neoplastic: Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).

149
Q

What are the non-infectious ways to get acute pericarditis? Metabolic?

A

Metabolic: Uraemia, myxoedema.

150
Q

What are the non-infectious ways to get acute pericarditis? Traumatic and Iatrogenic?

A

Traumatic and Iatrogenic: Early onset (rare): Direct injury (penetrating thoracic injury, oesophageal perforation). Indirect injury (non-penetrating thoracic injury, radiation injury).

151
Q

What are the non-infectious ways to get acute pericarditis? Delayed onset?

A

Delayed onset: Pericardial injury syndromes (common) iatrogenic trauma (e.g.coronary percutaneous intervention, pacemaker lead insertion and radiofrequency ablation).

152
Q

What are most cases of pericarditis?

A

Idiopathic.

153
Q

What is the clinical presentation of somebody with pericarditis?

A

Chest pain Severe Sharp and pleuritic (without constricting crushing character of ischaemic pain) Rapid onset Left anterior chest or epigastrium Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve) Relieved by sitting forward exacerbated by lying down Other symptoms Dyspnoea Cough Hiccups (phrenic) Systemic disturbance Viral prodrome, Antecedent fever Skin rash, joint pain, eye Sx, weight loss (Cause) PMH Cancer, Rheumatological Dx, Pneumonia, Cardiac procedure (PCI, ablation), MI.

154
Q

What is the differential diagnosis of pericarditis?

A

Pneumonia Pleurisy Pulmonary Embolus Chostocondritis Gastro-oesophageal reflux Myocardial ischaemia/infarction.

155
Q

What tests can you do to check if somebody has pericarditis?

A

Clinical examination Pericardial rub – pathognomonic, crunching snow Sinus tachycardia Fever Signs of effusion (pulsus paradoxus, Kussmauls sign) ECG Bloods CXR Echocardiogram.

156
Q

What does an ECG look like with a patient who has pericarditis?

A

Diffuse ST segment elevation. Concave ST segment - may resemble acute injury pattern of STEMI. No reciprocal ST depression. Saddle shaped. PR depression. Mechanism is epicardial inflammation as adjacent to pericardium (parietal is inert).

157
Q

What would blood tests show in tests of pericarditis?

A

FBC Modest increase in WCC, mild lympocytosis ESR & CRP High ESR may suggest aetiology ANA in young females - SLE Troponin Elevations suggest myopericarditis CXR Often normal in idiopathic Pneumonia common with bacterial Modest enlargement of cardiac silhouette rule out effusion (>300ml to be detectable!)

158
Q

What management can help with pericarditis?

A

Sedentary activity until resolution of symptoms and ECG/CRP Probably only applies to athletes - 3 months NSAID (Ibuprofen 600mg TDS PO 2/52) or Aspirin (750-1000mg BD PO 2/52) Colchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence.

159
Q

What is the most common cause of heart failure? What does this usually result from? What are some other causes?

A

Myocardial dysfunction. IHD. Hyoertension. Alcohol excess. Cardiomyopathy. Valvular. Endocardial. Pericardial causes.

160
Q

What is the difference between acute decompensated congestive heart failure and acute heart failure?

A

ADCHF: Generally <70 yrs Male dominance LVEF < 40% AHF: Mean age 71-76 yr 50% females 50% have LVEF>40%.

161
Q

What tests can you do for heart failure?

A

History and physical examination CXR/Blood Tests including NP. ECG. Echocardiography Myocardial perfusion imaging Specific blood tests Other forms of non-invasive and invasive imaging.

162
Q

What are the different types of cardiomyopathies?

A

Dilated. Hypertrophic. Restrictive. Right ventricular.

163
Q

What are the systems involved with protection and survival of the heart?

A

The sympathetic system. The renin-angiotensin-aldosterone axis. Inflammation.

164
Q

What does an increase in cardiac norepinephrine produce? What happens in the long term?

A

Gives support of the myocardial function. Altered Beta receptor transduction. Adverse effect on cardiac myocytes, Reduced myocardial reserve. Progressive myocardial dysfunction. THEREFORE increased heart failure.

165
Q

What does angiotensin 2 produce?

A

AT-II1 (Vasoconstriction Water and salt retention Cell proliferation Sympathetic activation) AT-112 (Vasodilatation Anti-proliferation).

166
Q

What are the symptoms of heart failure?

A

SOB, fatigue & ankle swelling) of heart failure are non-specific. More specific symptoms (orthopnoea & PND) are insensitive.

167
Q

What are the signs of heart failure?

A

Peripheral oedema, pul. Crackles & tachycardia are non-specific and of low predictive value. Raised JVP, S3 and displaced apex beat are specific but insensitive. Murmurs.

168
Q

What is the New York heart association classification for heart failure?

A

Class I: No limitation (Asymptomatic) Class II: Slight limitation (mild HF) Class III: Marked limitation (moderate HF) Class IV: Inability to carry out any physical activity without discomfort (severe HF).

169
Q

What are the heart failure stages?

A

A: High risk for developing HF B: Asymptomatic HF C: Symptomatic HF D: End-stage HF.

170
Q

What are the causes of acute decompensation of chronic heart failure?

A

AMI Uncorrected BP Obesity Superimp. infection AF & arrhythmias Excess alcohol Endocrine (DM/T4..) ve inotropes (Ca/beta) NSAIDS Treatment and Na+ noncompliance. Lack of information given to patient about diet, medications, etc.

171
Q

What are some complications of heart failure?

A

Renal dysfunction Rhythm disturbances (AF, Afl, VT, VF) Systemic thromboembolism* DVT & PE’s LBBB & Bradycardia Hepatic dysfunction Neurological + Psychological complications.

172
Q

What are diuretics used for mainly in heart failure?

A

Symptomatic relief of oedema and dyspnoea.

173
Q

What do ace inhibitors do?

A

Reduce morbidity and mortality of HF patients.

174
Q

What do aldosterone antagonists do?

A

Results in reduction of morbidity and mortality of heart failure patients. Beware of renal impairment and hyperkalaemia.

175
Q

What do beta blockers do?

A

Reduce morbidity and mortality.

176
Q

What do you do if there is heart failure with preserved left ventricular ejection fraction?

A

The current practice is to give diuretics to deal with the congestion. Treat any cardiovascular problem There may be a role for aldosterone antagonists (TOPCAT trial is awaited).

177
Q

How do valves and other structural diseases play into heart failure?

A

AS: AS+HF mean mortality is eminent, without surgery. AS and severe LVSD=the boat had been missed. MR: When LVEF becomes normal in MR, it is probably too late! MS AR

178
Q

What could be given to heart failure patients in the long run to help with re-synchronisation?

A

Multi-site pacemakers. Also add a defibrillator function.

179
Q

What is Tetralogy of Fallot?

A

Ventricular septal defects Pulmonary stenosis Hypertrophy of Rt Ventricle Overriding aorta.

180
Q

What are the physiology of Tetralogy of Fallot?

A

The stenosis of the RV outflow leads to the RV being at higher pressure than the left Therefore blue blood passes from the RV to the LV The patients are BLUE.

181
Q

How is Tetralogy of Fallot repaired?

A

The Blalock-Taussig Shunt 1944 Walter Lillehei first ‘complete repair’ on a boy aged 11 – rebore the RVOT and patch VSD 1986 first repair in infancy Now mostly repaired before the age of two years.

182
Q

What is Ventricular Septal Defects?

A

Abnormal connection between the two ventricles Common – 20% of all congenital heart defects – 1-4/1000 live births Many close spontaneously during childhood.

183
Q

What is the ventricular septal defects physiology?

A

Large Very high pulmonary blood flow in infancy Breathless, poor feeding, failure to thrive Require fixing in infancy (PA band, complete repair) May lead to Eisenmengers syndrome. Small Small increase in pulmonary blood flow only Asymptomatic Endocarditis risk Need no intervention.

184
Q

What are the ventricular septal defects clinical signs?

A

Large –Small breathless skinny baby –Increased respiratory rate –Tachycardia –Big heart on chest X ray –Murmur varies in intensity •Small –Loud systolic murmur –Thrill (buzzing sensation) –Well grown –Normal heart rate –Normal heart size.

185
Q

What is Eisenmengers syndrome?

A

High pressure pulmonary blood flow •Damages to delicate pulmonary vasculature •The resistance to blood flow through the lungs increases •The RV pressure increases •The shunt direction reverses •The patient becomes BLUE.

186
Q

What is atrial septal defect?

A

Abnormal connection between the two atria (primum, secundum, sinus venosus) •Common •Often present in adulthood.

187
Q

What is the physiology of atrial septal defects?

A

Slightly higher pressure in the LA than the RA •Shunt is left to right •Therefore NOT blue •Increased flow into right heart and lungs

188
Q

What is the physiology between large and small atrial septal defects?

A

Large –Significant increased flow through the right heart and lungs in childhood –Right heart dilatation –SOBOE –Increased chest infections –If any stretch on the right heart should be closed •Small –Small increase in flow –No right heart dilatation –No symptoms –Leave alone –NB. The shunt on small to moderate sized defects increases with age

189
Q

What are the clinical signs of atrial septal defects?

A

Pulmonary flow murmur •Fixed split second heart sound (delayed closure of PV because more blood has to get out) •Big pulmonary arteries on CXR •Big heart on chest X ray

190
Q

How can you close a ASD?

A

Surgical Percutamous (key hole technique).

191
Q

What can atria-ventricular septal defects involve?

A

Hole in the centre. Can involve the ventricular septum, the atrial septum, the mitral and tricuspid valves.

192
Q

What is the physiology of atria-ventricular septal defect? For a partial and complete defect?

A

Complete defect –Breathless as neonate –Poor weight gain –Poor feeding –Torrential pulmonary blood flow –Needs repair or PA band in infancy –Repair is surgically challenging •Partial defect –Can present in late adulthood –Presents like a small VSD / ASD –May be left alone if there is no right heart dilatation

193
Q

What is patent ductus arteriosus?

A

Failure of ductus arterioles to close.

194
Q

What are the clinical signs of ductus arterioles?

A

Continuous ‘machinery’ murmur •If large, big heart, breathless •Eisenmenger’s syndrome –Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)

195
Q

What is the physiology of patent ductus arterioles with a large and a small?

A

Large –Torrential flow from the aorta to the pulmonary arteries in infancy –Breathless, poor feeding, failure to thrive –More common in prem babies –Need to be closed (surgically) •Small –Little flow from the aorta to Pas –Usually asymptomatic –Murmur found incidentally –Endocarditis risk

196
Q

How do you close the ductus arterioles?

A

Surgical or percutaneous. Local anaesthetic. Venous approach.

197
Q

What is coarctation of the aorta?

A

Narrowing of the aorta at the site of insertion of the ductus arterioles.

198
Q

What is the physiology for coarctation of the aorta?

A

Severe –Complete or almost complete obstruction to aortic flow –Collapse with heart failure –Needs urgent repair •Mild –Presents with hypertension –Incidental murmur –Should be repaired to try to prevent problems in the long term

199
Q

What are the clinical signs of coarctation of the aorta?

A

Right arm hypertension •Bruits (buzzes) over the scapulae and back from collateral vessels •Murmur

200
Q

What are the long term problems of coarctation of the aorta?

A

Hypertension –Early coronary artery disease –Early strokes –Sub arachnoid haemorrhage •Re-coarctation requiring repeat intervention •Aneurysm formation at the site of repair

201
Q

What is bicuspid aortic valve? What are the problems associated with it?

A

Normal AV valves has three cusps. •Can be severely stenotic in infancy or childhood •Degenerate quicker than normal valves •Become regurgitant earlier than normal valves •Are associated with coarctation and dilatation of the ascending aorta

202
Q

What is pulmonary stenosis?

A

Narrowing of the outflow of the right ventricle. Valvar. Sub valvar. Supra valvar. Branch.

203
Q

What are the problems with pulmonary stenosis?

A

Severe –Right ventricular failure as neonate –Collapse –Poor pulmonary blood flow –RV hypertrophy –Tricuspid regurgitation •Moderate / mild –Well tolerated for many years –Right ventricular hypertrophy

204
Q

What is the treatment for pulmonary stenosis?

A

Treatment –Balloon valvuloplasty –Open valvotomy –Open trans-annular patch –Shunt (to bypass the blockage)

205
Q

What is a major risk factor for stroke, myocardial infarction, heart failure and chronic renal disease?

A

Hypertension.

206
Q

What is classified as hypertension?

A

140/90 mmHg.

207
Q

What are the mechanisms for BP control?

A

Cardiac output and peripheral resistance. Interplay between: Renin-Angiotensin-Aldosterone system. Sympathetic nervous system. Local vascular vasoconstrictor and vasodilator mediators.

208
Q

What does angiotensin 2 do?

A

Vascular growth - hyperplasia and hypertrophy. Salt retention - aldosterone release and tubular sodium reabsorption.

209
Q

What can you use against renin and ACE?

A

Renin inhibitor and ACE inhibitor.

210
Q

What does the sympathetic nervous system do?

A

Increase renin, peripheral resistance and cardiac output.

211
Q

How can you block the peripheral resistance of the sympathetic nervous system?

A

Alpha blocker

212
Q

How can you block the cardiac output of the sympathetic nervous system?

A

Beta blocker

213
Q

What are some examples of ACE inhibitors?

A

Ramipril and perindopril.

214
Q

What are the main clinical indications of ACE inhibitors?

A

Hypertension. Heart failure. Diabetic nephropathy.

215
Q

What are the main adverse effects of ACE inhibitors and why?

A
  1. Related to reduced angiotensin II formation a. Hypotension b. Acute renal failure c. Hyperkalaemia d. Teratogenic effects in pregnancy 2. Related to increased kinin production a. Cough b. Rash c. Anaphylactoid reactions
216
Q

What are the some examples of angiotensin 2 receptor blockers?

A

Candesartan and valsartan.

217
Q

What are the main clinical indications for angiotensin 2 receptor blockers?

A

Hypertension. Diabetic nephropathy. Heart failure.

218
Q

What are the main adverse effects of angiotensin 2 receptor blockers?

A

Symptomatic hypotension (especially volume deplete patients) Hyperkalaemia Potential for renal dysfunction Rash Angio-oedema Contraindicated in pregnancy Generally very well tolerated

219
Q

What are some examples of calcium channel blockers?

A

Amlodipine and nifedipine.

220
Q

What are the main clinical indications for calcium channel blockers?

A

Hypertension. Ischaemic heart disease (IHD) - angina. Arrhythmia.

221
Q

What are the different types of calcium channel blockers?

A

Dihydropyridines. Phenylalkylamines. Benzothiazepines.

222
Q

What do dihydropyridines affect?

A

Preferentially affect vascular smooth muscle. Peripheral arterial vasodilators.

223
Q

What do phenylalkylamines affect?

A

Main effects on the heart. Negatively chronotropic, negatively inotropic.

224
Q

What do benzodiazepines affect?

A

Intermediate heart/peripheral vascular effects.

225
Q

What are the adverse effects of calcium channel blockers?

A

1.Due to peripheral vasodilatation (mainly dihydropyridines) Flushing Headache Oedema Palpitations 2.Due to negatively chronotropic effects (mainly verapamil/diltiazem) Bradycardia Atrioventricular block 3.Due to negatively inotropic effects (mainly verapamil) Worsening of cardiac failure 4.Verapamil causes constipation

226
Q

What are some examples of beta-adrenoreceptor blockers?

A

Bisoprolol and carvedilol, propanolol.

227
Q

What are the main indications for beta-adrenoreceptor blockers?

A

Ischaemic heart disease. Heart failure. Arrhythmia. Hypertension.

228
Q

What are the main adverse effects of beta-adrenoreceptor blockers?

A

Fatigue Headache Sleep disturbance/nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction Worsening of: Asthma (may be severe) or COPD PVD – Claudication or Raynaud’s Heart failure – if given in standard dose or acutely

229
Q

What are the main clinical indications for diuretics?

A

Hypertension and heart failure.

230
Q

What are the different classes of diuretics?

A

Thiazides and related drugs (distal tubule). Loop diuretics (loop of Henle). Potassium-sparing diuretics. Aldosterone antagonists.

231
Q

What is an example of a thiazide and related diuretics?

A

Bendroflumethiazide

232
Q

What is an example of a loop diuretic?

A

Furosemide.

233
Q

What is an example of a potassium-sparing diuretic?

A

Spironolactone.

234
Q

What are the main adverse effects of diuretics?

A

Hypovolaemia (mainly loop diuretics) Hypotension ( “ ) Low serum potassium (hypokalaemia) Low serum sodium (hyponatraemia) Low serum magnesium (hypomagnesaemia) Low serum calcium (hypocalcaemia) Raised uric acid (hyperuricaemia – gout) Erectile dysfunction (mainly thiazides) Impaired glucose tolerance ( “ )

235
Q

What is the treatment for somebody with hypertension who is under the age of 55?

A

ACE-inhibitor or angiotensin 2 receptor blocker.

236
Q

What is the treatment for somebody with hypertension who is over the age of 55 or afro-caribbean any age?

A

Calcium channel blocker.

237
Q

What is step 2 if step 1 doesn’t work?

A

Use ACE-I / ARB and CCB.

238
Q

What is step 3 if step 2 doesn’t work?

A

ACE-I / ARB and CCB and Thiazide-like diuretic

239
Q

What is step 4 if step 3 doesn’t work?

A

Resistant hypertension. Consider action of spironolactone, high dose thiazide-like diuretic, alpha blocker, beta blocker.

240
Q

What is the symptomatic treatment of congestion?

A

Diuretics

241
Q

How do you treat heart failure?

A

Inhibition of renin-angiotensin-aldosterone system. Inhibition of sympathetic nervous system.

242
Q

What can you use to create the neurohumoral blockade?

A

ACE inhibitors Beta blocker. Aldosterone antagonists. Angiotensin receptor blocker. Hydralazine/nitrate combination.

243
Q

When are Atrial natriuretic peptide (ANP) - atria and B-(Brain) natriuretic peptide (BNP) – ventricles released?

A

Released by stretching of atrial and ventricular muscle cells Raised atrial or ventricular pressures Volume overload

244
Q

What are the main effects of ANP and BNP?

A

Increase renal excretion of sodium (natriuresis) and water (diuresis) Relax vascular smooth muscle (except efferent arterioles of renal glomeruli) Increased vascular permeability Inhibit the release or actions of: Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH) Counter-regulatory system to the renin-angiotensin system

245
Q

What are cardiac natriuretic peptides metabolised by?

A

Neutral Endopeptidase (NEP, neprilysin) NEP inhibition increases levels of natriuretic peptides.

246
Q

What is an example of a neprilysin inhibitor?

A

Sacubitril.

247
Q

What do nitrates do?

A

Arterial and venous dilators Reduction of preload and afterload Lower BP.

248
Q

What are nitrates mainly used for?

A

Ischaemic heart disease (angina) Heart failure.

249
Q

What are some examples of nitrates?

A

ISOSORBIDE MONONITRATE GTN SPRAY GTN INFUSION.

250
Q

What are the main adverse effects of nitrates?

A

Headache; GTN syncope (spray).

251
Q

What are the different types of angina?

A

Chronic stable angina Anginal chest pain Predictable Exertional Infrequent Stable ************** 2. Unstable angina / acute coronary syndrome (NSTEMI) Unpredictable May be at rest Frequent Unstable ************** 3. ST elevation Myocardial Infarction (STEMI) Unpredictable Rest pain Persistent Unstable.

252
Q

How do you treat stable angina?

A
  1. Antiplatelet therapy Aspirin Clopidogrel if aspirin intolerant 2. Lipid-lowering therapy Statins (simvastatin, atorvastatin, rosuvastatin, pravastatin) 3. Short acting nitrate: GTN spray for acute attack 4. First line treatment: Beta blocker or Calcium channel blocker 5. If intolerant: SWITCH 6. If not controlled:COMBINE 7. If intolerant or uncontrolled, consider monotherapy or combinations with: Long acting nitrate Ivabradine (inhibits If current) Nicorandil (K channel activator) Ranolazine (inhibits late inward sodium current)
253
Q

How do you treat unstable angina?

A
  1. Pain relief: GTN spray Opiates – diamorphine 2. Dual antiplatelet therapy: Aspirin plus ticagrelor or prasugrel or clopidogrel 3. Antithrombin therapy: Fondaparinux 4. Consider Glycoprotein IIb IIIa inhibitor (high risk cases): tirofiban, eptifibatide, abciximab 5. Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker 6. Lipid lowering therapy: Statins 7. Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist ************************* Most patients will undergo invasive management with coronary angiography and revascularisation (angioplasty or CABG)
254
Q

What is class 1 in the Vaughan Williams classification of anti arrhythmic drugs?

A

Class I: Sodium channel blockers Ia - disopyramide, quinidine, procainamide Ib - lidocaine, mexilitene Ic - flecainide, propafenone

255
Q

What is class 2 in the Vaughan Williams classification of anti arrhythmic drugs?

A

Class II: Beta adrenceptor antagonists - propranolol, nadolol, carvedilol (non-selective) - bisoprolol, metoprolol (β1-selective)

256
Q

What is class 3 in the Vaughan Williams classification of anti arrhythmic drugs?

A

Class III: Prolong the action potential - amiodarone, sotalol

257
Q

What is class 4 in the Vaughan Williams classification of anti arrhythmic drugs?

A

Class IV: Calcium channel blockers - verapamil, diltiazem

258
Q

What is Digoxin?

A

Antiarrhythmic drug.

259
Q

What does digoxin do?

A

Cardiac glycoside Inhibit Na/K pump Main effects are on the heart: Bradycardia (increased vagal tone) Slowing of atrioventricular conduction (increased vagal tone) Increased ectopic activity Increased force of contraction (by increased intracellular Ca)

260
Q

What are the side effects of digoxin? When is it used?

A

Narrow therapeutic range Nausea, vomiting, diarrhoea, confusion Used in atrial fibrillation (AF) to reduce ventricular rate response Use in severe heart failure as positively inotropic.

261
Q

What would you give a patient with prolonged QT interval?

A

Amiodarone.

262
Q

What would you give a patient with Polymorphic Ventricular Tachycardia?

A

Sotalol.

263
Q

What are the side effects of Amiodarone?

A

Interstitial pneumonitis Abnormal liver function Hyperthyroidism / Hypothyroidism Sun sensitivity Slate grey skin discolouration Corneal microdeposits Optic neuropathy

264
Q

What is the normal aortic valve area?

A

3-4 cm2

265
Q

When do aortic stenosis symptoms occur?

A

When the valve area is 1/4th of normal.

266
Q

What are the different types of aortic stenosis?

A

Supravalvular Subvalvular Valvular.

267
Q

What can congenital aortic stenosis occur with?

A

Unicuspid, bicuspid and tricuspid valve.

268
Q

What is congenital bicuspid valve associated with?

A

Aortic coarctation, dissection or aneurysm.

269
Q

What are some acquired aortic stenosis conditions?

A

Degenerative calcification. Rheumatic heart disease.

270
Q

What is rheumatic heart disease?

A

Fusion of cusps.

271
Q

How many of the population of bicuspid aortic valve and how much percentage of first degree relatives will have it?

A

0.5 - 2% and 10%.

272
Q

What is the pathophysiology of aortic stenosis?

A

A pressure gradient develops between the left ventricle and the aorta. (increased afterload) LV function initially maintained by compensatory pressure hypertrophy When compensatory mechanisms exhausted, LV function declines.

273
Q

What happens in aortic stenosis?

A

Simultaneous left ventricular (LV) and central aortic (Ao) pressures in a patient with aortic stenosis.

274
Q

What is the optimal way to measure the pressure difference?

A

The optimal way to measure the gradient in a patient with aortic stenosis is to use these simultaneous pressures.

275
Q

How does a person with aortic stenosis present?

A

Syncope: (exertional) 15% Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35% Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50% Sudden death <2%.

276
Q

What are the physical signs of aortic stenosis?

A

Syncope: (exertional) 15% Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35% Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50% Sudden death <2%

277
Q

What is the prognosis of aortic stenosis patients?

A

Angina + AS: 50% survive for 5 years. Syncope + AS: 50% survive for 3 years, HF + AS mean survival is <2 years. Risk of SCD in asymptomatic or minimally symptomatic patients is rare (<2%).

278
Q

What tests would you do for someone with aortic stenosis?

A

Echocardiography Two measurements obtained are: Left ventricular size and function: LVH, Dilation, and EF Doppler derived gradient and valve area (AVA).

279
Q

What is the gradient for grading of aortic stenosis?

A

Mild >1.5 2.6 m/s-3.0m/s Moderate 1.0-1.5 3.0 m/s-4.0 m/s Severe <1.0 >4.0m/s

280
Q

What is the management for aortic stenosis?

A

General: Fastidious dental hygiene / care Consider IE prophylaxis in dental procedures Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS Surgical Replacement: Definitive treatment TAVI – Transcatheter Aortic Valve Implantation

281
Q

What two different interventions do you do for asymptomatic and symptomatic patients?

A

Asymptomatic: Medical management and surveillance Symptomatic: AoV replacement (even in elderly and CHF)

282
Q

What is chronic mitral valve regurgitation?

A

Definition: Backflow of blood from the LV to the LA during systole Mild (physiological) MR is seen in 80% of normal individuals.

283
Q

What are the aetiologies of chronic mitral valve regurgitation?

A

Myxomatous degeneration (MVP) Ischemic MR Rheumatic heart disease Infective Endocarditis.

284
Q

What is the pathophysiology of mitral valve regurgitation?

A

Pure Volume Overload Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension. Progressive left ventricular volume overload leads to dilatation and progressive heart failure.

285
Q

What are the physical signs and symptoms of mitral valve regurgitation?

A

Auscultation: soft S1 and a pansystolic murmur at the apex radiating to the axilla S3 (CHF/LA overload) In chronic MR, the intensity of the murmur does correlate with the severity. Displaced hyperdynamic apex beat Exertion Dyspnoea: ( exercise intolerance) Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation.

286
Q

What do imaging studies for mitral regurgitation show?

A

ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR CXR: LA enlargement, central pulmonary artery enlargement. ECHO: Estimation of LA, LV size and function. Valve structure assessment TOE v helpful

287
Q

What are the medications/management for MR?

A

Vasodilator such as ACEI, hydralazine Rate control for atrial fibrillation with -blockers, CCB, digoxin Anticoagulation in atrial fibrillation and flutter Diuretics for fluid overload Serial Echocardiography: Mild: 2-3 years Moderate: 1-2 years Severe: 6-12 months IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

288
Q

What are the indications for surgery of severe MR?

A

ANY Symptoms at rest or exercise with (repair if feasible) Asymptomatic: If EF <60%, LVESD >45mm If new onset atrial fibrillation/raised PAP.

289
Q

What is the definition of aortic valve regurgitation?

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.

290
Q

What is the aetiology of chronic AR?

A

Bicuspid aortic valve Rheumatic Infective endocarditis.

291
Q

What is the pathophysiology of AR?

A

Combined pressure AND volume overload Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

292
Q

What would a pressure graph look like for aortic regurgitation?

A

Steep pressure drop after ventricles have contracted in the aorta.

293
Q

What are the physical exam findings of AR?

A

Wide pulse pressure: most sensitive Hyperdynamic and displaced apical impulse Auscultation- Diastolic blowing murmur at the left sternal border Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate Systolic ejection murmur: due to increased flow across the aortic valve

294
Q

What would cardiac tests show you?

A

CXR: enlarged cardiac silhouette and aortic root enlargement ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)

295
Q

What is the management for AR?

A

General: consider IE prophylaxis Medical: Vasodilators (ACEI’s improve stroke volume and reduce regurgitation only if pt symptomatic or HTN. Serial Echocardiograms: to monitor progression. Surgical Treatment: Definitive Tx

296
Q

What is mitral valve stenosis?

A

Definition: Obstruction of LV inflow that prevents proper filling during diastole

297
Q

What is the aetiology of mitral valve stenosis?

A

Rheumatic heart disease: 77-99% of all cases Infective endocarditis: 3.3% Mitral annular calcification: 2.7%.

298
Q

What is mitral valve stenosis pathophysiology?

A

Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying) worse with exercise, fever, tachycardia, and pregnancy Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. Right heart failure symptoms: due to Pulmonary venous HTN Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

299
Q

What are the physical signs of MS?

A

prominent “a” wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in advanced disease Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

300
Q

What are the heart sounds in MS?

A

Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex. Heard best with the patient lying on the left side in held expiration Intensity of the diastolic murmur does not correlate with the severity of the stenosis Loud Opening S1 snap: heard at the apex when leaflets are still mobile Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips. A shorter S2 to opening snap interval indicates more severe disease.

301
Q

What tests can you do on MS and what will they show?

A

ECG: may show atrial fibrillation and LA enlargement CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

302
Q

How would you manage a patient with MS?

A

Serial echocardiography: Mild: 3-5 years Moderate:1-2 years Severe: yearly Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression -blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling Duiretics for fluid overload

303
Q

What is infective endocarditis?

A

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc). It’s like a really bad infection, but with the added extras of showering infectious crap all around your bloodstream, and/or eating holes in your heart valves.

304
Q

What are the different types of infective endocarditis?

A

Left sided native IE (mitral or aortic) Left sided prosthetic IE Right sided IE (rarely prosthetic as rare to have PV or TV replaced) Device related IE (pacemakers, defibrillators, with or without valve IE Prosthetic; can be Early (within year) or Late (after a year) post op Each type can have different presentations, pathogens and outcomes.

305
Q

How do you catch infective endocarditis?

A

Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected. Introduce infectious material into the blood stream or directly onto the heart during surgery Have had IE previously

306
Q

Who does infective endocarditis affect?

A

the elderly (in an ageing population) the young i.v. drug abusers the young with congenital heart disease. Anyone with prosthetic heart valves.

307
Q

What is the clinical presentation of infective endocarditis?

A

Depends on site, organism, etc Signs of systemic infection (fever, sweats, etc) Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction Valve dysfunction; heart failure, arrythmia

308
Q

How do you diagnose somebody with infective endocarditis?

A

2 Major Criteria Bugs grown from blood cultures evidence of endocarditis on echo, or new valve leak 5 Minor Criteria Predisposing factors Fever Vascular phenomena Immune phenomena Equivocal blood cultures. Definite IE 2 major, 1 major+3 minor, 5 minor Possible IE 1 major, 1 major+3 minor, 5 minor.

309
Q

What test can you do for infective endocarditis?

A

ECG (ischemia or infarction, new appearance of heart block) Transthoracic echo (TTE). Safe, non-invasive, no discomfort, often poor images so lower sensitivity. Transoesophageal (TOE/TEE). Excellent pictures as long as you don’t mind having a big tube pushed down your throat. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration. Easiest if ventilated (but never ventilate just for TOE)

310
Q

What are some peripheral stigmata of infective endocarditis?

A

Petechiae 10 to 15%, Splinter hemorrhages Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits) Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole Roth spots on fundoscopy.

311
Q

How can you diagnose infective endocarditis?

A

Cultures may remain negative in 2% to 5% of patients with IE. Certain organisms: cell media; special media or microbiological methods, or may require long incubtion 7-21/7. The most common cause for negative blood cultures in patients with IE is prior antimicrobial therapy. WBC is rarely helpful. Raised CRP is almost always present.

312
Q

How can you treat infective endocarditis?

A

Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc Surgery.

313
Q

When do you operate on somebody with infective endocarditis?

A

the infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall) complications (aortic root abscess, severe valve damage to remove infected devices (always needed) to replace valve after infection cured (may be weeks/months/years later To remove large vegetations before they embolise

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