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Phase 2A > Cardiology > Flashcards

Cardiology Flashcards

1
Q

outline the RAAS system

A
  1. liver produces and secretes angiotensinogen
  2. kidney secretes renin (secretion is stimulated by low fluid volume moving through nephrons)
  3. renin converts angiontensinogen to angiotensin I
  4. angiotensin converting enzyme secreted by the lungs converts angiotensin I to angiotensin II
  5. ANG II causes ADH secretion, stimulates thirst and vasoconstriction and acts on the adrenal gland to produce aldosterone
  6. increase in blood pressure
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2
Q

cardiac output equation

A

CO = HR x Stroke Volume

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3
Q

Define angina.

A

Angina is a type of IHD. It is a symptom of O2 supply/demand mismatch to the heart experienced on exertion.

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4
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis.

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5
Q

Give 5 possible causes of angina.

A
  1. Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
  2. Increased distal resistance = LV hypertrophy.
  3. Reduced O2 carrying capacity e.g. anaemia.
  4. Coronary artery spasm.
  5. Thrombosis.
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6
Q

Give 5 modifiable risk factors for angina.

A
  1. Smoking.
  2. Diabetes.
  3. High cholesterol (LDL).
  4. Obesity/sedentary lifestyle.
  5. Hypertension.
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7
Q

Give 3 non-modifiable risk factors for angina

A
  1. Increasing age.
  2. Gender, male bias.
  3. Family history/genetics
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8
Q

What are the three main risk factors for IHD

A

Advancing age
Cigarette Smoking
Family history (first degree relatives who died of heart trouble under the age of 60)

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9
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.

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10
Q

Briefly describe the pathophysiology of angina that results from anaemia.

A

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 carrying capacity-> myocardial ischaemia -> angina.

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11
Q

How do blood vessels try and compensate for increased myocardial demand during exercise.

A

When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!

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12
Q

Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?

A

In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!

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13
Q

How can stable angina be reversed?

A

Resting - reducing myocardial demand.

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14
Q

How would you describe the chest pain in angina?

A

Crushing central chest pain. Heavy weight on chest

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15
Q

Give 5 symptoms of angina.

A
  1. Crushing central chest pain.
  2. The pain is relieved with rest or using a GTN spray.
  3. The pain is provoked by physical exertion.
  4. The pain might radiate to the arms, neck or jaw.
  5. Breathlessness.
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16
Q

What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?

A

Pre-test probability of CAD. It takes into account gender, age and typicality of pain.

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17
Q

What investigations might you do in someone you suspect to have angina?

A
  1. ECG - usually normal, there are no markers of angina.
  2. Echocardiography.
  3. CT angiography - has a high Negative Predictive Value (NPV) and is good at excluding the disease.
  4. Exercise stress test ECG - induces ischaemia.
  5. Invasive angiogram - tells you FFR (pressure gradient across stenosis).
  6. Blood tests (FBC, U&Es)
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18
Q

Describe the primary prevention of angina.

A
  1. Risk factor modification.

2. Low dose aspirin.

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19
Q

Describe the secondary prevention of angina.

A
  1. Risk factor modification (stop smoking, exercise, diet)
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events.
  3. Interventional therapies e.g. PCI.
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20
Q

Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.

A
  1. Beta blockers.
  2. Nitrates e.g. GTN spray (symptom relief)
  3. Calcium channel blockers.
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21
Q

Describe the action of beta blockers.

A

Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. This reduces cardiac output and so decreases oxygen demand

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22
Q

Give 3 side effects of beta blockers.

A
  1. Bradycardia.
  2. Tiredness.
  3. Erectile dysfunction.
  4. Cold peripheries.
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23
Q

When might beta blockers be contraindicated?

A

They might be contraindicated in someone with asthma or in someone who is bradycardic.

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24
Q

Describe the action of nitrates.

A

Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.

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25
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.

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26
Q

Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.

A
  1. Aspirin.

2. Statins.

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27
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!

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28
Q

What are statins used for?

A

They reduce the amount of LDL in the blood.

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29
Q

What is revascularisation?

A

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

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30
Q

Name 2 types of revascularisation.

A
  1. PCI (percutaneous coronary intervention)

2. CABG (coronary artery bypass graft)

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31
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive.
  2. Convenient and acceptable.
  3. High risk of restenosis.
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32
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery.
  2. Very invasive.
  3. Long recovery time.
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33
Q

Stable angina

A

Induced by exertion and relieved by rest

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34
Q

three environmental factors that can exacerbate angina

A

cold weather
heavy meals
emotional stress

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35
Q

how much stenosis does there have to be for angina to present

A

70% stenosis

rapidly declines

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36
Q

what is unstable angina

A

critical ischaemia but not quite so bad that it has caused an infarct
will have pain on rest

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37
Q

what is the gold standard investigation for angina

A

perfusion MRI

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38
Q

side effects of calcium channel blockers

A

flushing
postural hypotension
swollen ankles

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39
Q

how do statins work

A

HMG CoA reductase inhibitors (the enzyme that produces cholesterol)

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40
Q

when would you use a PCI

A

STEMI
NSTEMI
Stable angina

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41
Q

When would you use CABG

A

NSTEMI

Stable angina

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42
Q

Define atherosclerosis.

A

A hardened plaque in the intima of an artery. It is an inflammatory process.

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43
Q

What can an atherosclerotic plaque cause?

A
  1. Heart attack.
  2. Stroke.
  3. Gangrene.
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44
Q

What are the constituents of an atheromatous plaque?

A
  1. Lipid core.
  2. Necrotic debris.
  3. Connective tissue.
  4. Fibrous cap.
  5. Lymphocytes.
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45
Q

Give 5 risk factors for atherosclerosis.

A
  1. Family history.
  2. Increasing age.
  3. Smoking.
  4. High levels of LDL’s.
  5. Obesity.
  6. Diabetes.
  7. Hypertension.
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46
Q

In which arteries would you be most likely to find atheromatous plaques?

A

In the peripheral and coronary arteries.

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47
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

The media.

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48
Q

What is the precursor for atherosclerosis.

A

Fatty streaks.

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49
Q

What can cause chemoattractant release?

A

A stimulus such as endothelial cell injury.

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50
Q

What are the functions of chemoattractants?

A

Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!

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51
Q

Describe the process of leukocyte recruitment.

A
  1. Capture.
  2. Rolling.
  3. Slow rolling.
  4. Adhesion.
  5. Trans-migration.
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52
Q

Describe in 5 steps the progression of atherosclerosis.

A
  1. Fatty streaks.
  2. Intermediate lesions.
  3. Fibrous plaque.
  4. Plaque rupture.
  5. Plaque erosion.
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53
Q

Progression of atherosclerosis: what are the constituents of fatty streaks?

A

Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.

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54
Q

Progression of atherosclerosis: what are constituents of intermediate lesions?

A
  • Foam cells.
  • Smooth muscle cells.
  • T lymphocytes.
  • Platelet adhesion.
  • Extracellular lipid pools.
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55
Q

Progression of atherosclerosis: what are the constituents of fibrous plaques?

A
  • Fibrous cap overlies lipid core and necrotic debris.
  • Smooth muscle cells.
  • Macrophages.
  • Foam cells.
  • T lymphocytes.
    Fibrous plaques can impede blood flow and are prone to rupture.
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56
Q

Progression of atherosclerosis: why might plaque rupture occur?

A

Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.

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57
Q

What is the treatment for atherosclerosis

A

Percutaneous coronary intervention (PCI).

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58
Q

Major limitation of PCI

A

restenosis

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59
Q

How can restenosis be avoided following PCI?

A

Drug eluting stents: anti-proliferative and drugs that inhibit healing.

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60
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process!

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61
Q

Define atherogenesis.

A

The development of an atherosclerotic plaque.

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62
Q

What are acute coronary syndromes (ACS)?

A

ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI.

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63
Q

What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.

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64
Q

What are uncommon causes of ACS?

A
  1. Coronary vasospasm.
  2. Drug abuse.
  3. Coronary artery dissection.
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65
Q

Briefly describe the pathophysiology of ACS?

A

Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia and infarction -> necrosis of cells -> permanent heart muscle damage and ACS

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66
Q

what is the significance of troponin in ACS

A

when myocardial cells are damaged, troponins are released and enter the bloodstream
MIs have troponin rises, unstable angina does not

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67
Q

Describe type 1 MI.

A

Spontaneous MI with ischaemia due to plaque rupture.

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68
Q

Describe type 2 MI.

A

MI secondary to ischaemia due to increased O2 demand.

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69
Q

Why do you see increased serum troponin in NSTEMI and STEMI?

A

The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this.

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70
Q

Give three signs of unstable angina

A
  1. cardiac chest pain at rest
  2. cardiac chest pain with cresecendo pattern as pain has an increased frequency and severity
  3. new onset of angina occuring at rest
  4. no significant rise in troponin
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71
Q

diagnosis of unstable angina

A

history
ECG shows no clear evidence of MI
Troponin has no significant rise

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72
Q

why is there no significant rise of troponin in unstable angina

A

because there is no damage (infarction) to the heart only ischaemia

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73
Q

Give 6 signs/symptoms that are typical of an MI.

A
  1. Unremitting and usually severe central cardiac chest pain.
  2. Pain occurs at rest.
  3. Sweating
  4. Breathlessness.
  5. Nausea/vomiting.
  6. 1/3 occur in bed at night.
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74
Q

Give 5 potential complications of MI.

A
  1. Heart failure.
  2. Rupture of infarcted ventricle.
  3. Rupture of interventricular septum.
  4. Mitral regurgitation.
  5. Arrhythmias.
  6. Heart block.
  7. Pericarditis.
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75
Q

What investigations would you do on someone you suspect to have ACS?

A
  1. ECG.
  2. Blood tests; look at serum troponin.
  3. Coronary angiography.
  4. Cardiac monitoring for arrhythmias.
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76
Q

What might the ECG of someone with unstable angina show?

A

The ECG from someone with unstable angina may be normal or might show T wave inversion and ST depression.

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77
Q

What might the ECG of someone with NSTEMI show?

A

The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression. There also might be R wave regression, ST elevation and biphasic T wave in lead V3.

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78
Q

how do you diagnose a STEMI

A

ST-elevation can usually be diagnosed at the time of presentation on an ECG

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79
Q

What might the ECG of someone with STEMI show?

A

The ECG from someone with STEMI will show ST elevation in the anterolateral leads. After a few hours, T waves invert and deep, broad, pathological Q waves develop.

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80
Q

how do you diagnose an NSTEMI

A

retrospective diagnosis

troponin levels

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81
Q

A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

A
  1. Gram negative sepsis.
  2. Pulmonary embolism.
  3. Myocarditis.
  4. Heart failure.
  5. Arrhythmias.
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82
Q

what test can you do that is an indicator for heart failure?
where is it produced?
Why does it indicate HF?

A

B-type natriuretic peptide is a hormone that helps to regulate blood volume. Produced by the left ventricle. Heart releases more of this hormone when the left ventricle is stretched from having to work harder

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83
Q

Management of someone having an ACS

A 
Get to hospital ASAP!!! I STEMI call PCI centre for transfer 
ROMANCE
Reassure 
Oxygen (if hypoxic and below 94)
Morphine
Aspirin 300mg immediately
Nitrates 
Clopidogrel (ST elevation)
Enoxaparin (heparin)
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84
Q

What is the treatment of choice for STEMI?

A

PCI.

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85
Q

how does aspirin work as an antiplatelet drug

A

irreversibly inhibits prostaglandin H synthase in platelets and megakaryocytes blocking the formation of thromboxane A2

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86
Q

what happens if you inhibit the P2Y12 receptor

A

decreased thromboxane production and decreased platelet aggregation

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87
Q

What is the function of P2Y12?

A

It amplifies platelet activation.

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88
Q

what is dual antiplatelet therapy

A

aspirin + P2Y12 inhibitor

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89
Q

when is dual antiplatelet therapy used

A

management of ACS

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90
Q

three oral options of P2Y12 inhibitors

A

clopidogrel
prasugrel
ticagrelor

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91
Q

action of clopidogrel

A

binds to the P2Y12 receptor

to stop its effects have to wait until all the platelets have been replaced (10-12 days)

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92
Q

action of ticagrelor

A

binds reversibly to the P2Y12 receptor

its effects relate to the presence of the drug in the plasma

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93
Q

3 side effects of P2Y12 inhibitors

A

increased bleeding
rash
GI disturbances

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94
Q

Describe the secondary prevention therapy for people after having a STEMI.

A
  1. Aspirin.
  2. Clopidogrel (P2Y12 inhibitor).
  3. Statins.
  4. Metoprolol (beta blocker).
  5. ACE inhibitor.
  6. Modification of risk factors.
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95
Q

what other drug category can you use as well as antiplatelet drugs

A

anti-coagulants
used during PCI
enoxaparin (low molecular weight heparin)

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96
Q

what is the pathway of electrical activity in the heart

A

SA node –> R+L atrium –> AV node –> bundle of His –> R+L bundle branches –> Purkinje fibres (left bundle splits into post and anterior fascicle)

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97
Q

the chest leads look at the heart in what plane?

A

horizontal

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98
Q

the limb leads look at the heart in what plane?

A

vertical

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99
Q

what does V1 look at

A

septal aspect of the heart

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100
Q

what does V2, V3, V4 look at

A

anterior aspect of the heart

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101
Q

what does V5 and V6 look at

A

lateral aspect of the left ventricle

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102
Q

which lead has the best view of the heart

A

lead II

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103
Q

ECG: what is the normal axis of the QRS complex?

A

-30° -> +90°

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104
Q

what is left axis deviation

A

past -30°

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105
Q

ECG: what does the P wave represent?

A

Atrial depolarisation.

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106
Q

ECG: how long should the PR interval be?

A

120 - 200ms.

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107
Q

ECG: what might a long PR interval indicate?

A

Heart block.

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108
Q

what is right axis deviation

A

past +90°

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109
Q

how to decide if someone has left axis deviation or right axis deviation

A

The Axis was Left Two the Right One
Lead II = negative = LAD
Lead I = negative = RAD

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110
Q

3 causes of left axis deviation

A

Left anterior fascicular block
Left BBB
LVH

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111
Q

2 causes of right axis deviation

A

Left posterior fascicular block

right heart hypertrophy

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112
Q

equation to determine heart rate of a regular rhythm

A

rate = 300 / (number of large squares between R waves)

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113
Q

equation to determine rate of an irregular rhythm

A

rate = (QRS complexes in 10s) x 6

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114
Q

how many big squares on an ECG reading = 1 second

A

5

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115
Q

how many big squares on an ECG reading = 1 mV

A

2

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116
Q

what might M shaped P waves on an ECG suggest (p mitrale)

A

Left atrial hypertrophy

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117
Q

what might tall pointed p waves (p pulmonale) on an ECG suggest

A

right atrial hypertrophy

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118
Q

What is the dominant pacemaker of the heart?

A

The SA node. 60-100 beats/min.

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119
Q

How long should the QRS complex be?

A

Less than 110 ms.

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120
Q

In which leads would you expect the QRS complex to be upright in?

A

Leads 1 and 2.

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121
Q

In which lead are all waves negative?

A

aVR.

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122
Q

Give 3 signs of abnormal T waves

A
  1. Symmetrical.
  2. Tall and peaked.
  3. Biphasic or inverted.
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123
Q

What happens to the QT interval when HR increases?

A

The QT interval decreases.

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124
Q

define heart failure

A

an inability of the heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures

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125
Q

why are males more at risk of developing heart disease

A

do not have the protection that oestrogen provides

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126
Q

what is the most common cause of heart failure

A

ischaemic heart disease

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127
Q

name three causes of heart failure

A

hypertension
alcohol excess
cardiomyopathy

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128
Q

risk factors for developing heart failure?

Including ethnicity

A 
Over 65
Male 
Of african descent 
obesity
history of MI
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129
Q

pathophysiology of heart failure

A

DIAGRAM IN NOTES

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130
Q

Three symptoms of heart failure

A 
shortness of breath
fatigue
ankle swelling 
cold peripheries
increased weight
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131
Q

Name three signs of heart failure

A
  1. peripheral oedema
  2. raised jugular venous pressure
  3. S3 and S4 heart sounds
  4. Crackles and tachycardia
  5. Murmurs and displaced apex beat
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132
Q

Investigations for heart failure

A

Chest X-ray
Blood test : B-type natriuretic peptide
Echocardiography

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133
Q

What is the value of B-type natriuretic peptide that diagnoses heart failure

A

BNP > 400ng/L

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134
Q

Outline the New York Heart Association Classification

A

Class I : no limitation
Class II : slight limitation (milf HF), patient is comfortable at rest
Class III : marked limitation, less than ordinary activities causes dyspnoea which is limiting
Class IV: inability to carry out any physical activity without discomfort

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135
Q

Three examples of acute decompensation of chronic heart failure

A

acute MI
uncorrected increased BP
Obesity

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136
Q

Three complications of heart failure

A

Renal dysfunction
Arrhythmias
Systemic thromboembolism

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137
Q

Management of acute heart failure

A

Medical emergency

ROMANCE

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138
Q

Lifestyle management of chronic heart failure

A

Stop smoking
Stop drinking alcohol
Eat less salt
Optimize weight and nutrition

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139
Q

What hormones does the heart produce?

A

ANP and BNP

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140
Q

What are the functions of ANP and BNP?

A
  1. Increased renal excretion of Na+ and therefore water.
  2. Vasodilators.
  3. Inhibit aldosterone release.
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141
Q

What drugs can we use in the management of heart failure

A 
Diuretics (mainly symptomatic relief of oedema, usually loop diuretics) 
ACE-inhibitors 
Beta-blockers
Aldoesterone antagonist
Digoxin
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142
Q

What would you give if patient is intolerant to ACE-i

A

ARB (angiotensin II Receptor Blocker)

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143
Q

How does digoxin work?

A

It inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves.

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144
Q

What are the main effects of digoxin?

A
  1. Bradycardia.
  2. Reduced atrioventricular conduction.
  3. Increased force of contraction (positive inotrope).
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145
Q

Give 4 potential side effects of digoxin.

A
  1. Nausea.
  2. Vomiting.
  3. Diarrhoea.
  4. Confusion.
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146
Q

In what diseases is digoxin clinically indicated

A

Atrial fibrillation

LVSD

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147
Q

what drug is used to treat heart failure with preserved ejection fraction

A

Spironolactone

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148
Q

Hypertension is a major risk factor for what three conditions

A

Stroke
MI
Heart failure
Chronic renal disease

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149
Q

hypertension symptoms

A

asymptomatic!

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150
Q

signs of hypertension

A

high blood pressure
retinopathy
end organ damage (e.g proteinuria)

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151
Q

What is clinical high blood pressure defined as?

A

140/90mmHg or higher

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152
Q

If patients have suspected hypertension (have a clinical blood pressure) what is next offered?

A

Ambulatory blood pressure monitoring

153
Q

why are ABPM results slightly lower than clinical blood pressure readings

A

white coat hypertension

154
Q

definitions of stage 1 hypertension

A

clinical BP : 140/90

ABPM : 135/85

155
Q

definition of stage 2 hypertension

A

clinical BP : 160/100

ABPM: 150/95

156
Q

what are the two forms of hypertension

A

primary and secondary hypertension

157
Q

cause of primary hypertension

A

unknown

158
Q

cause of secondary hypertension

A

renal disease
endocrine disorders
pregnancy
drugs

159
Q

what would be your first line of treatment for an adult with diabetes and hypertension for the treatment of hypertension

A

ACE-i or ARB

160
Q

what would be your first line treatment for an adult without DM, under the age of 55 from white family origin

A

ACE-i or ARB

161
Q

what would be your first line of treatment in an adult who is aged 55 years or over or is from a Black African or African-Caribbean family origin?

A

Calcium channel blocker

162
Q

How can hypertension be treated?

A
  1. Lifestyle modification e.g. reduce salt intake.

2. Anti-hypertensive drugs.

163
Q

Write an equation for BP.

A

BP = CO X TPR.

164
Q

Name 2 systems that are targeted pharmacologically in the treatment of hypertension.

A
  1. RAAS.

2. Sympathetic nervous system (NAd).

165
Q

Give 4 functions of angiotensin 2.

A
  1. Potent vasoconstrictor.
  2. Activates sympathetic nervous system; increased NAd.
  3. Activates aldosterone = Na+ retention.
  4. Vascular growth, hyperplasia and hypertrophy.
166
Q

Give 3 ways in which the sympathetic nervous system (NAd) lead to increased BP.

A
  1. Noradrenaline is a vasoconstrictor = increased TPR.
  2. NAd has positive chronotropic and inotropic effects.
  3. It can cause increased renin release.
167
Q

Lifestyle modification in the treatment of hypertension

A 
reduce weight if obese 
reduce alcohol intake 
stop smoking 
control cholesterol 
reduce salt intake 
low-fat diet 
increase exercise
168
Q

what are the criteria for starting antihypertensive drug treatment

A

stage 1 hypertension: under age of 80 who have organ damage, established CVS, renal disease or diabetes
Offer treatment to anyone with stage 2 hypertension

169
Q

Name 3 ACE inhibitors

A
  1. Ramapril.
  2. Enalapril.
  3. Perindopril.`
170
Q

In what diseases are ACE inhibitors clinically indicated?

A
  1. Hypertension.
  2. Heart failure.
  3. Diabetic nephropathy.
171
Q

Give 4 potential side effects of ACE inhibitors.

A
  1. Hypotension.
  2. Hyperkalaemia.
  3. Acute renal failure.
  4. Teratogenic.
172
Q

Why do ACE inhibitors lead to increased kinin production?

A

ACE also converts bradykinin to inactive peptides. Therefore ACE inhibitors lead to a build up of kinin.

173
Q

ACE inhibitors: give 3 potential side effects that are due to increased kinin production.

A
  1. Dry chronic cough.
  2. Rash.
  3. Anaphylactoid reaction.
174
Q

You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?

A

ACE inhibitors lead to a build up of kinin. One of the side effects of this is a dry and chronic cough.

175
Q

Name three angiotensin receptor blockers

A

Candesartan
Valsartan
Iosartan
Irbesartan

176
Q

What are ARBs?

A

Angiotensin 2 receptor blockers.

177
Q

At which receptor do ARB’s work?

A

AT-1 receptor blocker

178
Q

In what diseases are ARBs clinically indicated?

A
  1. Hypertension.
  2. Heart failure.
  3. Diabetic nephropathy.
179
Q

When would you prescribe an ARB

A

If an ACE-i is contraindicated

Have developed a chronic dry cough from ACE-i

180
Q

When are ARBs contraindicated

A

pregnancy

181
Q

Give 4 potential side effects of ARBs.

A
  1. Hypotension.
  2. Hyperkalaemia.
  3. Renal dysfunction.
  4. Rash.
182
Q

Name 3 calcium channel blockers

A
  1. Amlodipine
  2. Nifedipine
  3. Felodipine
  4. Lacidipine
  5. Verapamil
  6. Diltiazem
183
Q

Clinical indications for CCB

A

Hypertension.

  1. IHD.
  2. Arrhythmia.
184
Q

Name 2 dihydropyridines and briefly explain how they work.

A

Dihydropyridines are a class of calcium channel blockers. Amlodipine and felodipine are examples of dihydropyridines. They are arterial vasodilators.

185
Q

Name a calcium channel blocker that acts primarily on the heart (phenylalkylamines)

A

Verapamil – it is negatively chronotropic and inotropic.

186
Q

Name a calcium channel blocker that acts on the heart and on blood vessels.

A

Diltiazem – acts on the heart and the vasculature.

187
Q

On what channels do calcium channel blockers work?

A

L type Ca2+ channels.

188
Q

Give 3 potential side effects that are due to the vasodilatory ability of calcium channel blockers.

A

Flushing.

  1. Headache.
  2. Oedema.
189
Q

Give a potential side effect that is due to the negatively inotropic ability of calcium channel blockers.

A

Worsening cardiac failure

190
Q

what is normal heart rate

A

60-100bpm

191
Q

what is bradycardia?

A

slow heart rate (less than 60bpm)

192
Q

Give three potential consequences of arrhythmias

A
  1. Sudden death.
  2. Syncope.
  3. Dizziness.
  4. Palpitations.
  5. Can also be asymptomatic.
193
Q

Define tachycardia

A

Heart rate that is over 100bpm

194
Q

what type of nervous system simulation leads to bradycardia

A

increased parasympathetic tone

decreased sympathetic tone

195
Q

what are the two broad categories of tachycardia

A
  1. Supra-ventricular tachycardia’s.

2. Ventricular tachycardia’s.

196
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

197
Q

Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?

A

Supraventricular tachycardias are often associated with narrow complexes.

198
Q

Name 3 examples of supra-ventricular tachycardias?

A

Atrial fibrillation
Atrial flutter
Atrioventricular junctional tachycardias

199
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles.

200
Q

Do ventricular tachycardia’s have narrow or broad QRS complexes?

A

Ventricular tachycardias are often associated with broad complexes.

201
Q

what type of nervous system stimulation can lead to tachycardias

A

Decreased parasympathetic tone or an increased sympathetic tone

202
Q

Pathology of atrial fibrillation>

A

There is a loss of atrial mechanical contraction.

Multiple waves of electrical activity bombard the AV node. The atria respond electrically by contracting but there is no coordinated mechanical action and only a proportion of the impulses are conducted to the ventricles. Leads to a state of atrial spasm.

203
Q

what is the main risk associated with atrial fibrillation?

A

embolic stroke

204
Q

Aetiology of AF? (name three causes)

A 
Idiopathic 
Hypertension
Heart failure
Coronary artery disease 
Valvular heart disease (especially mitral stenosis)
205
Q

Name three risk factors which increase your likelihood of developing AF?

A 
Older than 60
Diabetes 
Hypertension
Coronary artery disease
Prior MI 
Structural heart disease
206
Q

What are the symptoms of AF?

A

Palpitations
Dyspnoea
Chest pains
Fatigue

207
Q

Name 2 signs in AF?

A

Irregularly irregular pulse

S1 heart sounds

208
Q

What investigation would you do in a patient with AF? And what does it show?

A

ECG

  • No p waves
  • Irregular and rapid QRS complex
  • fine oscillation over the baseline
209
Q

What is used to calculate stroke risk and need for anticoagulation in AF patients?

A 
Use the CHA2DS2-VASc score to calculate stroke risk at the need for anticoagulation 
Congestive HF (1) 
Hypertension (1) 
Age greater or equal to 75 (2)
Diabetes (1) 
Stroke (2) 
Vascular disease (1) 
Age 65-75 (1) 
Sex: female (1)

If the score is 2 or more need anticoagulation

210
Q

What is the management in a patient with acute AF + adverse signs

A

ABCDE
Electrical cardioversion by DC shock + amiodarone if unsuccessful
Heparin

211
Q

What is the management in a stable patient with acute AF that started less than 48 hours ago?

A
  • Electrical cardioversion with DC shock
  • If this failed can give it medically via IV infusion of flecainide or amiodarone
  • Enoxaparin to minimize risk of thromboembolism
212
Q

What is the management in a stable patient with acute AF that started more than 48 hours ago?

A

Ventricular rate control, use either
Calcium Channel Blocker e.g Diltiazem or Verapamil
Beta blocker e.g bisoprolol

213
Q

What are the two strategies use to manage chronic AF?

A

Rate control

Rhythm control

214
Q

Outline the rate control strategy used to manage chronic AF?

A

First line = beta blocker or CCB monotherapy
Plus digoxin if doesn’t work
Then consider amiodarone

215
Q

What patients do you use rhythm control strategy to control chronic AF?

A

younger
symptomatic
active

216
Q

outline the rhythm control strategy to control chronic AF?

A

Either so elective DC cardioversion (electric shock) or elective pharmacological cardioversion (IV flecainide is first line, then IV amiodarone)

217
Q

What treatment can you give to patients that have infrequent, symptomatic AF?

A

Flecainide PRN tablets

218
Q

what other medication should some AF patients be on? Why?

A

Anticoagulation
- Warfarin
- DOACS (Rivaroxaban, apixaban, edoxaban)
To reduce the risk of embolic stroke

219
Q

What is atrial flutter?

What is the pathological mechanism behind it?

A

Fast but organised atrial rhythm with an atrial rate between 250-300bpm. Regular response of the ventricles

The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.

220
Q

Name one risk factor that increases likelihood of developing atrial flutter?

A

Atrial fibrillation

221
Q

Aetiology of atrial flutter?

A 
Idiopathic
Coronary heart disease
Obesity 
Hypertension 
Heart failure
COPD
Pericarditis 
Acute excess alcohol intoxication
222
Q

Symptoms of atrial flutter

A 
Palpitations
Breathlessness
Chest pain
Syncope
Fatigue
Dizziness
223
Q

Investigation in atrial flutter and what does it show?

A

ECG

Regular sawtooth like atrial flutter waves between QRS complexes due to continuous atrial depolarisation

224
Q

What is a regular sawtooth like pattern on an ECG suggestive of?

A

Atrial flutter

225
Q

Treatment of atrial flutter

A

Acute : electrical cardioversion but anticoagulate before with enoxaparin

Catheter ablation (creating a conduction block to try and restore rhythm and block offending re-rentrant wave)

Iv amiodarone to restore sinus rhythm and use a beta blocker to suppress any further arrhythmias

226
Q

What is the pathology of AV re-entrant tachycardia Wolff-Parkinson White Syndrome?

A

Type of AV reentrant tachycardia

Normal AV circuit and accessory circuit can transmit impulses from the atria to ventricles.

The accessory circuit can transmit impulses from the atria to the ventricle or from the ventricle to the atria. This can set up a re-entrant circuit and the electrical signal goes around this accessory circuit stimulating the atria and ventricles to contract causing tachycardia

227
Q

Aetiology of Wolff-Parkinson-White syndrome?

A

Accessory pathway results from the incomplete separation of the atria and ventricles during fetal development

228
Q

Symptoms of Wolff-Parkinson-White Syndrome?

A

Palpitations
Severe dizziness
Dyspnoea
Syncope

229
Q

Investigation in Wolff-Parkinson -White syndrome? What does it show?

A

ECG
Short PR interval
Wide QRS complex with a delta wave (start of the complex is sloped)

230
Q

What syndrome is suggestive of a delta wave on an ECG ad short PR interval?

A

Wolff-Parkinson-White Syndrome

231
Q

Treatment of Wolff-Parkinson-White Syndrome?

A

Patients that present with haemodynamic instability (hypotension and pulmonary oedema) require emergency cardioversion.

If the patient is stable can use vagal manoeuvres
Breath-holding
Carotid massage
Valsalve manoeuvre - abrupt voluntary increase in intra-abdominal pressure and intra thoracic pressure by straining

If unsuccessful : IV adenosine

Surgery: catheter ablation of the accessory pathway

232
Q

what is the pathology behind AVNRT?

A

There are slow and fast pathways. Signals from the SAN can be carried by the slow pathway and transmitted to the ventricles and then travel back up the fast pathway setting up a reentrant loop at the AV node

233
Q

Risk factors for developing an AVNRT syndrome?

A 
Exertion
Emotional Stress
Coffee
Tea
Alcohol
234
Q

Symptoms of AVNRT syndromes?

A

Rapid regular palpitations with abrupt onset and sudden termination
Chest pain
Breathlessness
Neck pulsations

235
Q

Investigation in AVNRT syndrome and what does it show?

A

ECG

  • QRS complexes will show typical BBB sometimes
  • Narrow complex tachycardia
  • P waves are either not visible (hidden by QRS) or appear both before and after the QRS complex
236
Q

Treatment for AVNRT?

A

Catheter ablation

237
Q

What is the difference between AV Heart Block and Bundle Branch Block

A

AV Block : block in the AV node or Bundle of His

BBB: Block lower down in the conduction system

238
Q

define first degree heart block

A

Every atrial depolarisation is followed by conduction to the ventricles but with delay

239
Q

Aetiology of first degree heart block

A

Hyperkalaemia
Myocarditis
Inferior MI
AVN blocking drugs (Beta blockers, CCB or digoxin)

240
Q

What does an ECG show in first degree heart block?

A

Prolongation of the PR interval to greater than 0.22 seconds

241
Q

What are the subtypes of AV node blocks?

A

First degree
Second degree
Third degree

242
Q

Pathology of first degree AV block?

A

Every atrial depolarisation is followed by conduction to the ventricles but with delay

243
Q

Aetiology of First degree heart block?

A

Hyperkalaemia
Myocarditis
Inferior MI
AVN blocking drugs (Beta blockers, CCB or digoxin)

244
Q

What does an ECG show of a patient with first degree heart block

A

Prolongation of the PR interval to greater than 0.22 seconds

245
Q

How is Second degree heart block classified?

A

Mobitz I

Mobitz II

246
Q

What is the difference in presentation between Mobitz I and Mobitz II second degree heart block?

A

Mobitz I: Light headedness, dizziness, syncope

Mobitz II: SOB, postural hypotension and chest pain

247
Q

Aetiology of Mobitz I heart block?

A

AVN blocking drugs, inferior MI

248
Q

Aetiology of Mobitz II heart block?

A

Anterior MI, mitral valve surgery, SLE, Rheumatic fever

249
Q

What would the ECG of a patient with Mobitz I heart block show?

A

longer PR interval until no QRS complex and resets

250
Q

What would the ECG of a patient with Mobitz II heart block show?

A

QRS complex is dropped after every other p wave

251
Q

What is the treatment for Mobitz II heart block? Why?

A

Pacemaker - high risk of developing sudden complete AV block

252
Q

What is AV Third Degree Heart Block?

A

Complete heart block.

All electrical activity fails to conduct to the ventricles.

253
Q

How come ventricular contractions are sustained in AV Third Degree Heart Block?

A

sustained by spontaneous escape rhythm which originates below the block

254
Q

What are the causes of AV Third degree heart block?

A

Structural heart disease
Ischaemic heart disease (acute MI)
Hypertension
Endocarditis

255
Q

What are the symptoms of third degree heart block

A 
Light headedness
Dizziness
Syncope
Fatigue 
Chest pain 
Bradycardia
256
Q

What investigations do you do in third degree heart block?

A

ECG

257
Q

What may the ECG show in a patient with third degree heart block?

A

P waves are completely independent of the QRS complex

Can have either a narrow complex escape rhythm or broad complex escape rhythm

258
Q

What is the difference between a narrow and broad complex escape rhythm?

A

Narrow complex escape rhythm
QRS complex less than 0.12 seconds
Block originates in the His bundle (more proximal to AV node)

Broad complex escape rhythm
B = below His
QRS complex is greater than 0.12 seconds

259
Q

What is the treatment for narrow complex escape rhythm third degree heart block?

A

Acute may respond to IV atropine

Chronic : permanent pacemaker `

260
Q

What is the treatment for broad complex escape rhythm third degree heart block?

A

Permanent pacemaker

261
Q

What is right bundle branch block?

A

Right bundle no longer conducts so ventricles do not contract together.
Late activation of the right ventricle

262
Q

Name 2 causes of right bundle branch block?

A

Pulmonary embolism
Ischaemic Heart Disease
Atrial/ventricular septal defect

263
Q

What does the ECG show in a patient with right bundle branch block?

A

MaRRoW
QRS complex looks like an M in lead VI
QRS complex looks like a W in V5 and V6

Splitting of the second heart sound

264
Q

What is left bundle branch block?

A

Late activation of the left ventricle

265
Q

Name a cause of left bundle branch block?

A

IHD

Aortic valve disease

266
Q

What does the ECG show in a patient with left bundle branch block?

A

WiLLiaM
QRS complex looks like a W in leads VI and V2
QRS complex looks like a M in leads V4, V5 and V6

Splitting of the second heart sound

267
Q

What is the pathology of prolonged QT syndrome?

A

Cardiac channelopathy.

Function of the cardiac ion channels lead to prolongation of ventricular action potential, lengthening the QT interval.

268
Q

Name 1 congenital cause and 2 acquired causes of prolonged QT syndrome?

A

Congenital :
Autosomal dominant condition Romano-Ward syndrome

Acquired
Hypokalaemia
Hypocalcaemia
Drugs ; amiodarone, tricyclic antidepressants 
Bradycardia 
Acute MI
269
Q

What symptoms may a patient with prolonged QT syndrome have?

A

Some people are asymptomatic and may only become aware of their condition after having an ECG

Syncope
Seizures
Palpitations

Can lead to cardiac arrest and death.

270
Q

What does the ECG show of a patient with prolonged QT syndrome?

A

Prolonged QT interval

longer than 440ms at a HR of 60bpm

271
Q

Treatment of prolonged QT syndrome?

A

Treat the underlying cause

IV isoprenaline

272
Q

What is a ventricular ectopic?

A

A premature beat that arises from an abnormal (ectopic) site in the ventricular myocardium.

273
Q

Aetiology of a ventricular ectopic beat?

A

Most common post MI arrhythmia

Can also occur in healthy patients and are relatively common

Hypokalaemia

274
Q

What are the symptoms of a ventricular ectopic beat

A

Usually asymptomatic, patients may be uncomfortable especially if it is happening frequently.

Pulse is irregular

Can feel faint or dizzy

275
Q

What complication can arise from a ventricular ectopic beat?

A

High burden ventricular ectopic can cause heart failure

276
Q

What is the pathology of ventricular tachycardia?

A

Rapid ventricular beating that results in inadequate blood filling of the ventricles. This results in a decreased cardiac output leading to a decrease in the amount of oxygenated blood that is circulated by the body.

277
Q

Aetiology of ventricular tachycardia?

A

Commonly idiopathic

278
Q

Symptoms of ventricular tachycardia?

A

Breathlessness
Chest pain
Palpitations
Light headed or dizzy

279
Q

What would the ECG show in a patient who had sustained ventricular tachycardia?

A

ECG shows rapid ventricular rhythm and a broad and abnormal QRS complex (greater than 0.14s)

280
Q

Treatment for ventricular tachycardia?

Treatment if sustained and unstable/stable?

A

Beta-blockers

If sustained

1. Hemodynamically unstable
Emergency electrical cardioversion 
2. Stable 
IV beta-blocker
IV amiodarone
281
Q

What is ventricular fibrillation?

A

Very rapid and irregular ventricular activation with no mechanical effect (no cardiac output, no meaningful contraction)

282
Q

Aetiology of ventricular fibrillation?

A

Usually caused by a ventricular ectopic beat

283
Q

signs of ventricular fibrillation?

A

Patient is in cardiac arrest.
Pulseless
Unconscious
Respiration ceases

284
Q

What does the ECG show of a patient in ventricular fibrillation?

A

Shapeless, rapid oscillations

No hint of organised complexes

285
Q

Treatment for ventricular fibrullation?

A

Electrical defibrillation

Survivors are at an increased risk of sudden death so long term, implantable cardioverter - defibrillators are the first line therapy

286
Q

What is sinus tachycardia?

A

Conduction occurs as normal but impulses are initiated at a higher frequency

287
Q

What can cause sinus tachycardia?

A 
Anaemia 
Anxiety 
Exercise
Pain
Heart failure 
Pulmonary embolism
288
Q

What number of bpm = tachycardia?

A

Over 100bpm

289
Q

What are the symptoms of sinus tachycardia?

A

Fast heart rate
Difficulty breathing
Fainting
Dizziness

290
Q

What is an aortic aneurysm?

A

An artery with a dilatation of over 50% of its original diameter.

291
Q

What is the difference between true and false aneurysms?

A

True aneurysms : abnormal dilatations that involve ALL layers of the arterial wall

False aneurysms : involve a collection of blood in the outer layer only (adventitia)

292
Q

What is the pathology of aortic aneurysms?

A

Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss.

293
Q

Where are aortic aneurysms most commonly found?

A

infrarenal abdominal aorta

294
Q

What are aortic aneurysms associated with?

A 
Smoking 
Hypertension
Family History 
Marfan’s Syndrome 
Ehlers-Danlos syndrome 
Trauma 
Arteriomegaly (familial)
295
Q

What are the three ways that an abdominal aortic aneurysm can present

A

Asymptomatic
Symptomatic
Ruptured

296
Q

What are the symptoms/signs of an abdominal aortic aneurysm?

A

Central abdominal pain
Back pain
Distal embolic events
Pulsatile abdominal swelling

297
Q

How does a ruptured abdominal aortic aneurysm present?

A 
Severe and sudden onset epigastric pain 
Sudden unexplained hypotension 
Unexplained collapse 
Sweating associated with pulsatile abdominal mass 
Tachycardia
Profound anaemia
Sudden death
298
Q

What investigations happen if an AAA is detected?

A

If an aneurysm is detected then patient should be monitored with 6monthly abdominal US scans until the AAA reaches a diameter greater than 5.0cm.
Then CT angiogram

299
Q

What is the management for an AAA

A

Patient should be monitored with regular US scans until it reaches a diameter greater than 5.0cm.

Modify risk factors : stop smoking, healthy diet, control blood pressure, lower lipid

300
Q

Once an AAA reaches a diameter greater than 5.0cm what are the two surgical options for repair?

A

Endovascular aneurysm repair : placing a stent graft inside the aneurysm

Open repair: replace the aneurysmal section of the aorta with a new prosthetic graft.

301
Q

What is the emergency management of a ruptured AA?

A 
ECG
Take blood for amylase, Hb and cross match
Catheterize bladder
IV access with 2x large bore cannulae 
Treat shock with O-ve blood 
Prophylactic antibiotics 
Emergency repair
302
Q

Define a thoracic aortic aneurysm?

A

focal dilatation of the thoracic aorta to more than 1.5 times its normal diameter

303
Q

What is associated with thoracic aortic aneurysms?

A

Strong genetic link
Connective tissue disorders such as Marfan’s syndrome, Ehlers-Danlos syndrome

Weight lifting, cocaine and amphetamine use

304
Q

What are the symptoms of thoracic aortic aneurysms?

A

Most TAAs are asymptomatic

Pain/pressure in chest
Thoracic back pain
Aortic regurgitation
Difficulting swallowing (due to compression of the oesophagus)
Acute pain
Collapse, shock and sudden death if ruptures

305
Q

What investigations do you do with somebody who has a TAA?

A

CT chest with contrast
MRI chest
Transoesophageal echocardiography can be useful for identifying aortic dissection
Ultrasound

306
Q

What is the treatment for a TAA?

A

Regular monitoring for asymptomatic TAAs every 6 months by CT

Surgery : endovascular stent grafting repair or open repair

Surgery is needed for ruptured TAA or a symptomatic TAA

Reduce cardiovascular risk factors

307
Q

What is the pathology of an aortic dissection?

A

Tear in the intimal lining of the aorta which allows a column of blood under pressure to enter the aortic wall forming a haematoma which separates the intima from the adventitia. This forcing of the layers of the vessel apart results in dissection

308
Q

What are the majority of aortic dissections?

A

Type A dissections (ascending aorta)

309
Q

Name 3 causes of an aortic dissection

A

Inherited
Familial thoracic aortic aneurysm type 1 and 2
Marfan’s syndrome
Ehlers-Danlos syndrome

Degenerative
Atherosclerosis
Inflammatory
Trauma: shearing stresses in a RTA

310
Q

What are the symptoms of aortic dissection?

A

Sudden onset of severe chest pain, classically described as tearing pain

Other symptoms may occur which are a direct result of occlusion of smaller arteries by the dissecting process

  • Angina
  • Paraplegia
  • Limb ischaemia
  • Pulse deficit
311
Q

What are the signs of aortic dissection?

A
  • Hypertension
  • Pain is abrupt in onset and maximal at the time of onset
  • Pain migrates as the dissection progresses
  • Sharp/tearing pain
  • Patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord
312
Q

What investigations are done in an aortic dissection?

A

ECG
To distinguish from an MI
May be evidence of acute MI or acute ischaemia

MRI confirms a diagnosis

Transthoracic / transesophageal ultrasound will give an indication of site and extent of dissection

313
Q

What is the treatment for aortic dissection?

A

Urgent antihypertensive medication

  • IV labetalol or esmolol
  • CCB can be used if beta blocker is contraindicated

Morphine

Surgery
Endovascular intervention with stents
Open repair

314
Q

What is the pathology of intermittent claudication?

A

Partial blockage of leg/peripheral vessels by an atherosclerotic plaque/thrombus resulting in insufficient perfusion of the lower limb leading to lower limb ischaemia when exercising.

315
Q

what is the cause of intermittent claudication?

A

Atherosclerosis.

316
Q

what are the symptoms of intermittent claudication?

A

Cramping pain in the calf, thigh or buttock after walking for a given distance (claudication distance)
Pain is relieved by rest
Male impotence

317
Q

A patient experiences intermittent claudication pain in the calf. Where is the likely blockage?

A

Femoral artery disease

318
Q

A patient experiences intermittent claudication pain in the buttock. Where is the likely partial blockage?

A

iliac disease

319
Q

What are the signs of intermittent claudication?

A 
Pale
Cold leg with hair loss
May be poorly healing wounds of the extremities 
Pulseless
Paraesthesia
320
Q

What investigations do you do for intermittent claudication?

A

Blood tests
ECG
Ankle brachial pressure index
Imaging

321
Q

What blood tests do you do for intermittent claudication and critical ischaemia?

A 
HbA1c - exclude diabetes 
ESR and CRP - exclude arthritis
FBC - anaemia, polycythaemia
U&Es
Lipids
322
Q

What is is Ankle brachial pressure index (ABPI) ? What value defines intermittent claudication?
What value defines critical ischaemia?

A

Measurement of the cuff pressure at which blood flow is detectable by Doppler in the posterior tibial arteries compared to the brachial artery
Normal : 1-1.2
Intermittent claudication: 0.5-0.9
Critical Ischaemia: less than 0.5

323
Q

What imaging do you do in a patient with intermittent claudication/critical ischaemia?

A

Colour duplex ultrasound
If considering intervention MR/CT angiography is used to identify the extent and location of stenoses and quality of distal vessels

324
Q

What is the management of intermittent claudication?

A

Risk factor modification
Stop smoking
Treat hypertension, hyperlipidemia, diabetes
Clopidogrel to prevent progression and minimise risk
Exercise and weight loss

Supervised exercise programmes to reduce symptoms by improving collateral blood flow

Vasoactive drugs e.g naftidrofuryl oxalate

325
Q

What is critical ischaemia?

A

Partial blockage of leg/peripheral vessels by an atherosclerotic plaque/thrombus resulting in insufficient perfusion of the lower limb leading to lower limb ischaemia when exercising and at rest.

326
Q

Cause of critical ischaemia?

A

Atherosclerosis.

327
Q

What are the symptoms of critical ischaemia?

A

Severe unremitting pain in the foot, particularly at night

Pain can be partially relieved by hanging the foot out of the bed (gravity)

328
Q

Signs of critical ischaemia?

A 
Pallor
Perishingly cold 
Pain
Pulseless
Paresthesia
Paralysis 
Ulceration
Gangrene
329
Q

Treatment of critical ischaemia?

A

Risk factor modification
Stop smoking
Treat hypertension, hyperlipidemia, diabetes
Clopidogrel to prevent progression and minimise risk
Exercise and weight loss

Supervised exercise programmes to reduce symptoms by improving collateral blood flow

Revascularisation
Percutaneous transluminal angioplasty
Surgical reconstruction with a bypass graft

Amputation if severe, may relieve intractable pain and death from sepsis and gangrene.

330
Q

What is pericarditis?

A

An inflammatory pericardial syndrome with or without pericardial effusion

331
Q

What is the most common cause of pericarditis?

A

Viral infection

enteroviruses, herpesviruses

332
Q

aside from infectious causes, what other causes of pericarditis are there?

A 
- Neoplastic (second most common cause!) 
Metastatic tumours (lung, breast, cancer, lymphoma)
  • Idiopathic
  • Autoimmune (RA)
  • Metabolic (anorexia nervosa)
333
Q

Symptoms of pericarditis?

A 
Chest pain 
Severe
Central 
Sharp and pleuritic in nature 
Rapid onset 
Radiates to arm 
Relieved by sitting forward 
Exacerbated by lying down 
Dyspnoea 
Cough 
Hiccups (potential irritation to phrenic nerve)

Systemic disturbance : fever, headache, nausea, vomiting

334
Q

What is a pathognomonic sign of pericarditis?

A

Pericardial friction rub

335
Q

What does an ECG show in a patient with pericarditis?

A

Saddle ST elevation
PR depression
(Sinus tachycardia)

336
Q

What investigations do you do in a patient with pericarditis?

A

ECG

Bloods: FBC
Increase in WCC

High ESR may suggest a cause

Troponin : elevations suggest myopericarditis

CXR : identify a cause

Cardiovascular MR/CT may show localised inflammation

337
Q

Treatment of pericarditis?

A

Treat the cause !

NSAID
Ibuprofen
Aspirin

Gastric protection

Colchicine reduces recurrence but is not very well tolerated

338
Q

What is infective endocarditis?

A

Infection of the heart valves or other endocardial lined structures within the heart (such as septal defects, pacemakers, surgical patches)

339
Q

What is the most common type of infective endocarditis?

A

Left sided native

340
Q

Name 2 bacterial causes of infective endocarditis?

A

Strep. Viridans
Staph. Aureus (commonly in acute, native valves)
Enterococci
Coxiella burnetii

341
Q

Name one fungal cause of infective endocarditis? What patients do these more commonly present in?

A

Candida
Aspergillus
Histoplasma
Usually in IV drug abusers, immunocompromised

342
Q

Name three risk factors that increase a person’s likelihood of developing infective endocarditis?

A 
Skin breaches 
Renal failure 
Immunosuppression 
Diabetes 
IV drug abusers 
Anyone with a prosthetic heart valve
343
Q

Name the signs of infective endocarditis?

A

New murmur
Vegetations (infected mass)
Petechiae
Splinter haemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules usually found on the pulp of the digits)
Janeway lesions (erythematous, macular, nontender lesions on the fingers, palm or sole of the feet)
Roth spots on fundoscopy (dark ring with a pale centre)

344
Q

What complications can arise from infective endocarditis?

A

complication caused by a embolisation of collection of infective organism and their inflammatory mechanisms in organs: stroke, pulmonary embolism, bone infections, kidney dysfunction, MI

345
Q

What investigations do you do in a patient with infective endocarditis?

A

Bloods, raised CR, cultures
ECG: ischaemia, infarction, new appearance of first degree or worse heart block
Echocardiography (Transthoracic or transesophageal to detect vegetation)

346
Q

What is the first line treatment for infective endocarditis?

A

IV Antimicrobials for 6 weeks - choice is based on culture sensitivities

347
Q

What surgical treatment is there for patients with infective endocarditis?

A

Infection cannot be cured with antibiotics
ALWAYS to remove infected devices
Replace valve after the infection is cured
Remove large vegetations before they embolise

348
Q

what can cause aortic stenosis?

A

Congenital bicuspid valve which can progress to stenosis

Age related degenerative calcification

349
Q

What are the signs of aortic stenosis?

A

Crescendo-decrescendo ejection systolic murmur

Slow rising carotid pulse and decreased pulse amplitude

350
Q

what are the symptoms of aortic stenosis?

A

Syncope on exertion
Angina
Dyspnoea

351
Q

What investigation is diagnostic of aortic stenosis?

A

Echocardiography is diagnostic!

352
Q

What investigations do you in a patient with aortic stenosis?

A 
ECG
LVH
P-mitrale
Poor R wave progression
Complete AV block

CXR
LVH
Calcified aortic valve

353
Q

What is the treatment for aortic stenosis ?

A

Surgical replacement using a mechanical or bioprosthetic valve.

Procedure: Transcatheter Aortic Valve Implantation

354
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole.

355
Q

What can mitral regurgitation lead to?

A

Leads to left atrial enlargement and then progressive left ventricular volume overload leads to dilatation and progressive heart failure.

356
Q

Aetiology of mitral regurgitation?

A
  • Annular calcification
  • Mitral valve prolapse
  • Ruptured Chord of Mitral Valve
  • Dilated heart so there is a hole between the LA and LV and the leaflets will never close
  • Ischaemic MR caused by coronary disease - rupture or weakening of mitral valve
  • Infective endocarditis
357
Q

Symptoms of mitral regurgitation?

A

Exertion dyspnoea
Heart failure which may coincide with increased haemodynamic burden
Fatigue
Palpitations

358
Q

Signs of mitral regurgitation

A

Pansystolic murmur at the apex radiating to the axilla

Displaced hyperdynamic apex beat

359
Q

Investigations for mitral regurgitation?

A

ECG
CXR
Echo

360
Q

Treatment for mitral regurgitation?

A

Vasodilator (ACE-i, hydralazine)
Rate control for AF
Anticoagulation in AF and atrial flutter
Diuretics for fluid overload

Serial echo

IE prophylaxis for patients with prosthetic valves or a history of IE for dental procedures

361
Q

What is sepsis?

A

Infection with any organism can cause acute vasodilation from inflammatory cytokines

Life threatening organ dysfunction

362
Q

Name two organisms that commonly can cause sepsis?

A

coagulase-negative Staphylococcus and E. coli,

363
Q

What are the red flags to look out for in sepsis?

A 
Responds only to voice or pain/ unresponsive
Acute confusional state
Systolic BP < 90mmHg 
Heart rate > 130 per minute 
Respiratory rate > 25 per minute 
Needs oxygen to keep SpO2 > 92% 
Non-blanching rash, mottled/ashen/cyanotic
Not passed urine in the last 18hr 
Lactate > 2mmol/L
364
Q

What investigations do you do for sepsis ?

A 
Blood gas for lactate
Observations 
HR
BP
RR
O2 sats
Temperature
ECG
Urine dip 
Urine output monitoring 
Blood cultures 
U&amp;Es
CRP
FBC
LFT
Clotting screen
365
Q

Management/treatment of sepsis?

A

Early recognition and treatment is key!

Administer Oxygen
Aim to keep above 94%
88-92% if ar risk of CO2 retention (COPD)

IV Antibiotics
Broad spectrum
Start within 1 hour
Consider allergies

IV Fluids
If hypotensive/lactate > 2mmol/L give 500mL

Manage acute complications
Critical care review

366
Q

What type of reaction is anaphylaxis?

A

Type 1 IgE mediated hypersensitivity reaction.

367
Q

What is the pathology of an anaphylactic shock?

A

When a person is first exposed - sensitisation
Allergen interacts with B cells (B cells create antibodies). Antibodies are created in response to the antigen - IgE.
IgE attaches to mast cells.
The next time a person is exposed to allergen, the allergen attaches to IgE on the mast cells.
This activates the mast cells
Mast cells release cytokines (causing WBC recruitment)
Activation of mast cells and immune cells causes release of histamine

368
Q

What is the effect of histamine in anaphylaxis?

A

Histamine is a vasodilator
Causes large drop in blood pressure due to widespread vasodilation

The vessels also become leaky, which causes widespread oedema

369
Q

Name some examples of common allergens which can cause anaphylaxis?

A

Foods: peanuts, brazil, cashews, shellfish, dairy products
Venoms: wasps, bee, hornets
Medications: antisera (tetanus, diphtheria), latex, penicillin, aspirin, NSAIDs

370
Q

What are the signs and symptoms of anaphylaxis?

A 
Swelling (facial and laryngeal oedema) 
Bronchospasms
Hypotension
Rash - urticaria 
Central cyanosis
Wheezing 
Cardiac arrest 
Tachycardia 
Hypotension
371
Q

What is the first line treatment for anaphylaxis?

A

0.5mg adrenaline IM and repeat every 5 minutes if shock persists

372
Q

What is the management of anaphylaxis?

A

Administer IV antihistamine slowly
Administer 100mg intravenous hydrocortisone
If hypotension persists give 1-2L of IV fluid
If hypoxia is severe consider ventilation

373
Q

What is the action of giving adrenaline in an anaphylactic shock?

A

Beta adrenergic receptor activity
B1: increase heart rate and contractility
B2: bronchodilation

Alpha adrenergic receptor activity
A1: vasoconstriction, thus increasing peripheral vascular resistance and increasing blood pressure
A2: reduces further release of substances from mast cells by increasing intracellular cAMP

374
Q

What is the action of IV antihistamine in the treatment of an anaphylactic shock?

A

Inverse agonist of H1 receptor (so elicits the opposite response)
Blocks histamine so no…
- Vasodilation, hypotension, flushes, headaches, bradycardia, bronchoconstriction, increased vascular permeability

Weak antagonist of muscarinic ACh receptors 
Inhibit parasympathetic effects 
Increase heart rate 
May induce smooth muscle contraction 
Dry out secretions
375
Q

Action of IV hydrocortisone? Anaphylaxis

A

Immunosuppressive effects
Inhibits the release of histamine from mast cells and increases body’s response to circulating catecholamines (so enhances effects of adrenaline)

376
Q

What are the mediators involved in the allergic response? What are their roles?

A

Preformed mediators

  • Histamine and serotonin
  • Bronchoconstriction
  • Increased vascular permeability - capillary leak
  • Neutrophil and eosinophilic chemotactic factors
  • Induce inflammatory cell infiltration

Newly formed mediators

  • Chemoattractants
  • Prostaglandins and thromboxanes - platelet activating factor and prolonged airway hyperactivity. PAF levels correlate directly with severity of anaphylaxis
377
Q

What makes an allergen so powerful?

A

Many allergens are proteolytic, allowing them to cross skin and mucosal barriers. They are often aerodynamic particles which allow them to get in nasal and bronchial mucosa.

378
Q

Name an antihistamine

A

Chlorphenamine

379
Q

What confirmatory blood test is needed to take to confirm anaphylaxis has occurred?

A

Mast Cell Tryptase

Anaphylaxis causes an elevated serum mast cell tryptase.

Phase 2A (11 decks)

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