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Phase 2a Sheffield Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Define atherosclerosis

A

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

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2
Q

Define Atherogenesis

A

development of an atherosclerotic plaque

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3
Q

Where does plaque build up?

A

In the peripheral and coronary arteries

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4
Q

What is seen as a precursor to atherosclerosis?

A

Fatty streaks

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5
Q

What can Atherosclerotic plaque cause?

A
  1. Heart attack
  2. Gangrene
  3. Stroke
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6
Q

What are the constituents of atherosclerotic plaque?

A
  1. Lipid core
  2. Necrotic debris
  3. Connective tissue
  4. Fibrous Cap
  5. Lymphocytes
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7
Q

Give 5 risk factors for atherosclerosis

A
  1. Family history
  2. Age
  3. Smoking
  4. High LDLs
  5. Obesity
  6. Diabetes
  7. Hypertension
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8
Q

Which layer is thinned by atheromatous plaque?

A

The media

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9
Q

What is the role of a chemo-attractant?

A

Signal to leukocytes which accumulate and migrate into vessel walls -> Cytokine release

This causes inflammation

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10
Q

What triggers chemoattractants?

A

A stimulus such as endothelial injury.

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11
Q

What are the 5 steps of atherosclerotic progression?

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaque
  4. Plaque rupture
  5. Plaque erosion
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12
Q

What is the process of leukocyte recruitment?

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Adhesion
  5. Trans migration
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13
Q

What does the fatty streak consist of?

A

Foam cells and T lymphocytes

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14
Q

What do intermediate lesions consist of?

A

Foam cells, T lymphocytes, smooth muscle, platelet adhesion and EC lipid pools

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15
Q

What do fibrous plaque consist of?

A

Cap overlies lipid core and necrotic debris, macrophages, foam cells, T lymph

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16
Q

Why are Fibrous plaque’s prone to rupture and what is the consequence?

A

The FP constantly grows and recedes, the Fibrous cap must be reabsorbed and redeposited

If balance is shifted in favour of inflammatory conditions, cap becomes weak and plaque ruptures

Consequence - thrombus and vessel occlusion = impeding blood flow.

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17
Q

What is the treatment for atherosclerosis?

A

Percutaneous coronary intervention (PCI)

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18
Q

What is a limitation of PCI?

A

The risk of restenosis.

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19
Q

What is done to minimise the risk of restenosis post PCI?

A

Using Drug-eluting stents –> anti proliferative and drugs that inhibit healing to prevent restenosis

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20
Q

What can be used to prevent atherosclerosis?

A

Aspirin as it is a platelet cyclooxygenase inhibitor

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21
Q

What is Angina?

A

Mismatch of oxygen demand and supply experienced on exertion. A type of IHD.

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22
Q

What is the main cause of Angina?

A

Most common cause is narrowing of the coronary arteries due to atherosclerosis

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23
Q

Describe the pathophysiology of angina.

A

On exertion there’s an increased O2 demand, blood flow obstructed by plaque

This causes myocardial ischaemia –> angina.

Can be reversed by resting.

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24
Q

List 5 causes of Angina

A
  1. Narrowed coronary artery
  2. Increased Distal resistance = LV hypertrophy
  3. Reduced O2 carrying capacity – anaemia
  4. Coronary artery spasm
  5. Thrombosis
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25
Q

List 5 modifiable risk factors for angina.

A
  1. Smoking
  2. Diabetes
  3. High cholesterol
  4. Obesity/sedentary lifestyle
  5. Hypertension
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26
Q

List 3 non modifiable risk factors

A
  1. Age
  2. Male
  3. Family history/genetics
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27
Q

What happens to microvascular resistance and flow when myocardial demand increases.

A

Microvasc resistance decreases

flow increases

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28
Q

What happens to microvascular resistance in a patient with CV disease

A

Epicardial resistance is high so Microvasc resistance drops at rest to compensate.

When exerted it cannot drop any lower = angina

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29
Q

How might a patient present with Angina?

A

Centralised crushing pain, heavy and tight

May get worse with cold weather, stress and heavy meals.

Always gets worst post exertion.

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30
Q

Give 3 symptoms of Angina

A
  1. Crushing central chest pain
  2. Pain is relieved at rest or using a GTN spray
  3. Pain is provoked by physical exertion
  4. Pain may radiate to arms, neck or jaw
  5. Breathlessness
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31
Q

What investigations could be considered for Angina?

A
  1. ECG – usually normal
  2. CT Angiography – has a high NPV and is good at excluding disease.
  3. Exercise tolerance test – induce ischaemia
  4. Invasive angiogram – tells you FFR – pressure gradient across stenosis
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32
Q

What test would you do to decide which investigation may be the best?

A

Pre test probability of CAD –> considers gender, age and typicality of pain.

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33
Q

What pharmacological therapies are used for Angina?

A
  1. Beta blockers
  2. Nitrates
  3. Calcium channel blockers
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34
Q

How do beta blockers work?

A

Antagonise sympathetic action –> neg inotropic and chronotropic

Can cause bradycardia, tiredness and erectile dysfunction.

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35
Q

When shouldn’t you give someone beta blockers?

A

If they have bradycardia or asthma

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36
Q

How do Nitrates work?

A

Venodilator –> decreased venous return –> decreased preload and less myocardial demand

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37
Q

How do calcium channel blockers work?

A

Arteriodilators –> reduced bp –> reduced afterload –> reduced myocardial demand

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38
Q

What primary prevention measure could be taken for Angina?

A

Risk factor modification and low dose aspirin

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39
Q

What secondary prevention measures could be taken for angina?

A

Risk factor modification, pharmacological therapies, interventional therapies e.g. PCI

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40
Q

What drugs can be used to improve the prognosis of someone at risk of angina?

A

Statins - Reduce amount of LDL in the blood.

Aspirin - COX inhibitors, prevents TXA2 Platelet aggregation (CAN CAUSE GASTRIC ULCERATION)

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41
Q

Define Revascularisation

A

Restores patent coronary artery and increases blood flow e.g. PCI and CABG

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42
Q

Two advantages of PCI and one disadvantage

A

Less invasive, convenient and acceptable

Risk of restenosis

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43
Q

One advantage and two disadvtanges of CABG

A

Advantage - very effective

Disadvantage - Very invasive, long recovery time

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44
Q

What is DVT?

A

A blood clot that develops within a deep vein in the body, usually the leg.

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45
Q

What are the symptoms of DVT?

A 
Nonspecific symptoms
Pain and swelling	
Tenderness
Warmth
Slight discolouration
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46
Q

What investigations would you order in DVT?

A

D-dimer – look for breakdown of fibrin products, if normal it excludes DVT

Ultrasound compression scan – if you can’t squash the vein it’s a clot.

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47
Q

What is the treatment of DVT?

A
  1. LMWH
  2. Oral Warfarin or DOAC (direct oral anti-coag)
  3. Compression stockings
  4. Treat underlying cause e.g. malignancy
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48
Q

What are the risk factors for DVT?

A
  1. Surgery, immobility, leg fracture
  2. OCP,HRT
  3. Long Haul flights
  4. Genetic predisposition
  5. Pregnancy
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49
Q

How can you prevent DVT?

A
  1. Hydration
  2. Mobilisation
  3. Compression stockings
  4. Low dose LMWH (Low weight molecular heparin
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50
Q

What is the consequence of a dislodged DVT?

A

PE

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51
Q

How would you describe an Arterial thrombus?

A

platelet rich - white thrombosis

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52
Q

How would you describe a venous thrombus?

A

Fibrin rich - red thrombosis

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53
Q

Give 3 consequences of Arterial thrombosis

A
  1. MI
  2. Stroke
  3. Peripheral vasc disease-e.g. gangrene
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54
Q

How would you treat an arterial thrombus?

A

Aspirin, LMWH, Thrombolytic therapy

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55
Q

What are the consequences of Venous Thrombosis?

A

PE

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56
Q

How does warfarin work?

A

It is an agonist of Vit K and produces non functional clotting factors 2,7,9,10

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57
Q

Why is warfarin difficult to use?

A

Constant monitoring
Lots of interactions
Teratogenic

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58
Q

What is a Pulmonary embolism?

A

A blood clot that has broken off and traveled to the lung.

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59
Q

What are the symptoms of PE?

A

Breathlessness
Pleuritic chest pain
SOB

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60
Q

What are the signs of PE?

A

Tachycardia, tachypnoea, pleural rub.

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61
Q

What can PE Cause?

A

Hypotension
Cyanosis
severe dyspnoea
Right sided heart failure/strain

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62
Q

What investigations would you order for a PE?

A
  1. CXR normal, ECG Tachy
  2. ABG – Type 1 resp failure, decreased O2 and CO2
  3. Normal D-dimer excludes diagnosis
  4. Ventilation perfusion scan – mismatch defects
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63
Q

What is the treatment for PE?

A

LMW Heparin, oral warfarin, DOAC, treat cause if possible.

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64
Q

How can you prevent a PE?

A
  1. Hydration
  2. Mobilisation
  3. Compression stockings
  4. Low dose LMWH (Low weight molecular heparin)
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65
Q

What is acute pericarditis?

A

inflammatory pericardial syndrome with or without effusion.

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66
Q

What is the major differential diagnosis?

A

Myocardial infarction

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67
Q

What are the symptoms of acute pericarditis?

A
  1. Chest pain –> sharp, pleuritic, rapid onset pain radiates to the arm
  2. Dyspnoea
  3. Cough
  4. Hiccups – caused by irritation of phrenic nerve
  5. Skin rash
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68
Q

Why does cardiac tamponade sometimes occur in pericarditis?

A

The parietal pericardium can adapt when effusions accumulate

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69
Q

What are the causes of pericarditis?

A
  1. Viral (Enteroviruses)
  2. Bacterial e.g. Mycobacterium TB
  3. Autoimmune e.g. RA
  4. Neoplastic
  5. Metabolic e.g. Uraemia
  6. Traumatic and iatrogenic
  7. Idiopathic
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70
Q

What investigation would you do for pericarditis?

A
  1. ECG
  2. CXR
  3. Bloods
  4. Echocardiogram
  5. FBC, CRP, Cardiac enzymes
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71
Q

What would the ECG show?

A

ECG –> PR depression, saddle shaped ST elevation

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72
Q

What must a patient have to make a diagnosis of pericarditis?

A

Patient must have at least two of the following:

  • Friction rub
  • Chest pain
  • ECG changes
  • Pericardial effusion
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73
Q

How would you treat pericarditis?

A
  1. Avoid strenuous activity until symptoms resolve
  2. NSAID or aspirin – high doses
  3. Colchicine – anti inflammatory
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74
Q

What is haemopericardium?

A

Direct bleeding from vasculature through ventricular wall post MI

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75
Q

What is dresslers syndrome?

A

A secondary form of pericarditis

  • Myocardial injury stimulates auto-antibodies against the heart
  • Causes fever, chest pain and a pericardial rub (Occurs 2-10 weeks after MI )
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76
Q

What is giant cell arteritis?

A

Vasculitis, localised, chronic and granulomatous inflammation of the temporal arteries.

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77
Q

Signs of Giant cell arteritis?

A

Thickened often palpable blood vessels

Evidence of granulomatous inflammation

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78
Q

What is a consequence of giant cell arteritis?

A

Blindness if the occular artery is affected

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79
Q

What criteria is used to diagnose IE?

A

The duke criteria.

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80
Q

What is infective endocarditis?

A

Infection of the heart valves or other endocardial lined structure within the heart

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81
Q

Describe the pathogenesis of IE

A

Microbial adherence –> vegetation on valve –> cardiac valve distortion

Causes cardiac failure and septic problems

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82
Q

What is the hallmark of IE?

A

Vegetation - lumps of fibrin hanging off heart valves

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83
Q

What are the causes of IE?

A
  1. Staph Aureus
  2. Staph Epidermis (Coagulase neg staph)
  3. Strep Viridians (alpha haemolytic)
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84
Q

Where are vegetations likely to grow?

A

Atrial surface of AV valves and ventricular surface of SL valves

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85
Q

Who is at risk of Infective endocarditis?

A

Elderly, IVDU, Those with rheumatic fever and Those with prosthetic valves

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86
Q

What are the risk factors for IE?

A
  1. Having a regurgitant or prosthetic valve

2. If infectious material is introduced into the blood stream during surgery

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87
Q

What are the symptoms of IE?

A
  1. Signs of systemic infection
  2. Embolization e.g. stroke, pe, mi
  3. Valve dysfunction e.g. HF or arrhythmia
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88
Q

What are the signs of IE?

A

splinter haemorrhages, oslers nodes, jaenway lesions, roth spots, heart murmurs

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89
Q

What investigations should be done if IE is suspected?

A
  1. Blood culture
  2. Echocardiogram shows endocardial involvement
  3. Bloods – raised ESR/CRP
  4. ECG
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90
Q

Give one disadvantage and two advantages of Transthoracic echo’s

A

Poor images, but safe and nnon invasive

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91
Q

Give one advantage and two disadvtanges of transoesophageal echos

A

Good pictures, discomfort, perforation + aspiration possible

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92
Q

What criteria is used for diagnosing infective endocarditis?

A

Dukes criteria

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93
Q

How do you treat infective endocarditis?

A
  1. Antibiotic based cultures
  2. Treat any complications
  3. Surgery
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94
Q

What are the different types of Infective endocarditis?

A
  1. Left sided native IE
  2. Left sided prosthetic IE
  3. Right sided IE
  4. Device related IE
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95
Q

True of false - Left sided IE is more likely to cause thrombo emboli.

A

True

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96
Q

True of false - Right sided IE is more likely to spread to the lungs.

A

True.

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97
Q

What are some indications for surgery in a patient with IE?

A
  • AB not working
  • Complications
  • To remove infected devices
  • To replace the valve
  • To remove large vegetations before they embolise
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98
Q

What is the standard treatment of Myocardial infarction?

A
  • MONA - Morphine,oxygen,nitrogen,aspirin
  • PCI
  • Aspirin and clopidogrel
  • LMWH
  • Anti-anginals –> Beta blockers, CCB, nitrates
  • Prevent secondary event
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99
Q

What is the secondary prevention measures for NSTEMI?

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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100
Q

What is an acute coronary syndrome?

A

A spectrum of acute coronary conditions including unstable angina, NSTEMI and STEMI.

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101
Q

What is the commonest cause of ACS?

A

Rupture of atherosclerotic plaque and subsequent arterial thrombosis

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102
Q

What are uncommon causes of ACS?

A

Coronary Vasospasm
Drug abuse
Coronary artery dissection

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103
Q

What are the two types of Myocardial infarction?

A

M1 - Spontaneous MI with ischaemia due to plaque rupture

M2 - MI secondary to ischaemia due to increased O2 demand

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104
Q

What are the 3 cardiac enzymes?

A

Troponin
CK
Myoglobin

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105
Q

When are cardiac enzymes released?

A

During MI - during myocardial necrosis.

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106
Q

When is Troponin increased?

A

During MI - both NSTEMI and STEMI as a result of an occlusion causing ischaemia

Not significantly in angina
Can be in pericarditis but less so than an MI.

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107
Q

Other than an MI, when can Troponin be released?

A
  • Gram negative sepsis
  • Pulmonary embolism
  • Myocarditis
  • Heart failure
  • Arrhythmia
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108
Q

What is a STEMI?

A

ST elevated myocardial infarction

Characteristed by ST elevation in anterolateral leads, Inverted T waves and Q waves become broad.

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109
Q

What is an NSTEMI?

A

Non ST elevated myocardial infarction

Can only be diagnosed after bloods (raised troponin)

ECG may be normal or show T wave inversion and ST depression.

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110
Q

What is unstable angina?

A

Type of IHD, Acute, poor blood flow to the heart characteristed by chest pain at rest.

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111
Q

What are the signs of unstable angina?

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo patterns – pain more frequent and easily provoked
  3. No significant rise in troponin.
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112
Q

What is the treatment for unstable angina?

A

Clopidogrel, aspirin, surgery, lifestyle changes

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113
Q

What is the ECG like in unstable angina?

A

Normal or T wave inversion and ST depression

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114
Q

What are the signs of a Myocardial infarction?

A
  • Unremitting and severe cardiac chest pain
  • Pain that radiates down the left arm
  • Pain occurs at rest
  • Sweating, breathlessness, nausea and or vomiting
  • 1/3rd occur in bed at night.
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115
Q

What are the complications for Myocardial Infarction?

A
  • Heart failure
  • Rupture of infarcted ventricle
  • Rupture of interventricular septum
  • Mitral regurgitation
  • Arrythmias
  • Heart block
  • Pericarditis
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116
Q

A patient presents with an ACS, what investigations should be ordered?

A
  1. ECG
  2. Blood tests – troponin
  3. Coronary angiography
  4. Cardiac monitoring for arrythmias
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117
Q

A patient is diagnosed with ACS, what management options should be explored?

A
  1. Hospital
  2. If STEMI – PCI centre for transfer
  3. Aspirin 300mg, pain relief – morphine
  4. Oxygen if hypoxic
  5. Nitrates
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118
Q

What does P2Y12 do?

A

Amplifies platelet aggregation

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119
Q

What is a P2Y12 inhibitor?

A

Clopidogrel

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120
Q

What are some side effects of P2Y12 inhibitors?

A

Bleeding
Rashes
GI distrubances

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121
Q

What are the four types of valvular heart disease?

A
  1. Aortic Stenosis
  2. Mitral regurgitation
  3. Mitral stenosis
  4. Aortic regurgitation
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122
Q

What is aortic stenosis?

A

where the aortic orifice is restricted, and the LV can’t eject blood properly in systole –> pressure overload

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123
Q

What is the aetiology of aortic stenosis?

A
  1. Congenital bicuspid valve
  2. Acquired e.g. age-related degenerative calcification
  3. Rheumatic heart disease
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124
Q

What is the pathophysiology of aortic stenosis?

A
  1. Aortic orifice is restricted so there’s a pressure gradient between the aorta and LV
  2. LV function is maintained due to compensatory hypertrophy
  3. Overtime this leads to LV failure
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125
Q

What are the symptoms of aortic stenosis?

A
  1. Exertional syncope
  2. Angina
  3. Exertional dyspnoea (difficult or laboured breathing)
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126
Q

What are the signs of aortic stenosis?

A
  1. Slow rising carotid plus due to decreased pulse amplitude
  2. Soft or absent heart sounds
  3. Ejection systole murmur
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127
Q

What investigations would you order for aortic stenosis?

A

Echocardiography

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128
Q

What is the correct management for aortic stenosis?

A
  1. Ensure good dental hygiene
  2. Consider IE Prophylaxis
  3. Aortic Valve replacement or TAVI
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129
Q

Who should be offered an aortic valve replacement in aortic stenosis?

A
  1. Symptomatic patients with aortic stenosis
  2. Any patient with decreasing ejection fraction
  3. Any patient undergoing CABG with moderate aortic stenosis
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130
Q

Why does medication not work for mitral and aortic stenosis?

A

Medication doesn’t work for mitral and aortic stenosis as problem is mechanic so doesn’t prevent progression.

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131
Q

What is mitral regurgitation?

A

Back flow of the blood from LV to LA during systole – LV volume overload

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132
Q

What is the aetiology of mitral regurgitation?

A
  1. Myxomatous degeneration
  2. Ischaemic mitral regurgitation
  3. Rheumatic heart disease
  4. IE
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133
Q

What is the pathophysiology of mitral regurgitation?

A
  1. LV volume overload
  2. Compensatory mechanisms – LA enlargement and LVH and increased contractility
  3. Progressive LV volume overload causes dilation and progressive heart failure
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134
Q

What are the symptoms of Mitral regurgitation?

A
  1. Dyspnoea on exertion

2. Heart failure

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135
Q

What are the signs of mitral regurgitation?

A
  1. Pansystolic murmur
  2. Soft 1st heart sound
  3. 3rd heart sound
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136
Q

What is a sign of MR getting worse?

A

The intensity of the murmur

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137
Q

What are the investigations in Mitral regurgitation?

A
  1. CXR
  2. ECG
  3. Echocardiogram – estimate LA/LV size and function
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138
Q

What is the management of Mitral regurgitation?

A
  1. Rate control for AF –> Beta blockers
  2. Anticoagulation for AF
  3. Diuretics for fluid overload
  4. IE prophylaxis
  5. If symptomatic –> Surgery
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139
Q

What is aortic regurgitation?

A

A regurgitation aortic valve means blood leaks back into the LV during systole due to ineffective aortic cusps.

140
Q

What is the aetiology of Aortic regurgitation?

A
  1. Bicuspid aortic valve
  2. Rheumatic heart disease
  3. IE
141
Q

What is the pathophysiology of Aortic regurgitation?

A
  1. Pressure and volume overload
  2. Compensatory mechanisms –>LV dilation, LVH
  3. Progressive dilation eventually leads to Heart failure
142
Q

What are the symptoms of Aortic regurgitation?

A
  1. Dyspnoea on exertion
  2. Orthopnoea – breathlessness when lying down
  3. Palpitations
  4. Paroxysmal nocturnal dyspnea
143
Q

What are the signs of aortic regurgitation?

A
  1. Wide pulse pressure
  2. Diastolic blowing murmur
  3. Systolic ejection murmur
144
Q

What investigations would you take in aortic regurgitation?

A

CXR

Echocardiogram

145
Q

What is the management of Aortic regurgitation?

A
  1. IE prophylaxis
  2. Vasodilators e.g. ACEi
  3. Regular echocardiograms to monitor progression
  4. Surgery if symptomatic
146
Q

What is mitral stenosis?

A

Obstruction to LV inflow that prevents proper filling during diastole

147
Q

What are the causes of mitral stenosis?

A
  1. Rheumatic heart disease
  2. IE
  3. Calcification
148
Q

What is the pathophysiology of Mitral stenosis?

A
  1. LA dilation –> pulmonary congestion
  2. Increased trans mitral pressures  LA enlargement and AF
  3. Pulmonary venous hypertensions cause RHF symptoms
149
Q

What are the symptoms of mitral stenosis?

A
  1. Dyspnea
  2. Haemoptysis
  3. RHF symptoms
150
Q

What are signs of mitral stenosis?

A
  1. A wave in jugular venous pulsations
  2. Signs of RHF
  3. Pink patches on cheeks due to vasoconstriction
  4. Low pitched diastolic murmur
  5. Loud opening 1st heart sound snap
151
Q

What are the investigations for mitral stenosis?

A
  1. ECG
  2. CXR
  3. Echocardiogram – gold standard
152
Q

What is the management of mitral stenosis?

A
  1. If in AF –> Beta blockers/CCB
  2. If in AF –> anticoagulation
  3. Balloon valvuloplasty or valve replacement
  4. IE prophylaxis
153
Q

What is a main symptom of hypertension?

154
Q

Does treatment improve symptoms of hypertension?

A

Not usually, but may help headaches.

155
Q

What are the causes of hypertension?

A
  1. Kidney disease
  2. Genetics and family history
  3. Lifestyle factors e.g. high salt, excess alcohol, obesity, stress and caffeine
  4. Recreational drugs
  5. Drugs such as OCP and NSAIDs
  6. Hyperaldosteronism
156
Q

What endocrine diseases can cause secondary hypertension?

A
  1. Conn’s – hyperaldosteronism
  2. Cushing’s syndrome – prolonged cortisol exposure –> raised bp
  3. Pheochromocytoma –> adrenal gland tumour, excess NAd and Ad release
157
Q

What could you examine in a patient with suspected Hypertension?

A

Eyes in hypertension – small exposed blood vessels due to high bp.

158
Q

What investigations would you do in someone with suspected hypertension?

A
  1. 24h ambulatory blood pressure monitoring to confirm diagnosis
  2. ECG and blood tests may be done to identify secondary causes of hypertension
159
Q

What is hypertension a risk factor to?

A
  1. MI
  2. Stroke
  3. Heart failure
  4. Chronic renal disease
  5. Dementia
160
Q

What is the target levels of treatment in hypertension?

A

Under 80s - 140/90

Over 80s - 150/80

161
Q

When would you start treating people with hypertension?

A

Low risk - 160/100

High risk - 140/90

162
Q

What is the ABCD Management for hypertension?

A

A – ACEi .g. Rampiril or ARB e.g. candesartan if ACEi Intolerant

B – beta blockers e.g. bisoprolol

C – Calcium CB e.g. amlodipine or verapamil

D – Diuretics – Bendroflumethiazide

163
Q

What are the side effects of ramirpil?

A
  1. Hypotension
  2. Cough, rash due to increased kinin production
  3. Hyperkalaemia
  4. Teratogenic
  5. Acute renal failure
164
Q

What does Valsartan act on?

A

on AT-1 and prevents Ang 2 Binding

165
Q

What are the side effects of valsartan?

A

hypotension, renal dysfunction, hyperkalaemia, rash and contraindicated in pregnancy

166
Q

What are the side effects of bisoprolol

A
  • Hypotension
  • Fatigue
  • Headaches
  • Nightmares
  • Bradycardia
  • Hypotension
  • Erectile dysfunction
  • Cold peripheries
167
Q

What are the side effects of amlodipine?

A

flushing,headache, oedema, palpitations

168
Q

What are the side effects of Verapamil?

A

bradycardia, AV block (caused by neg chronotropic) and worsening cardiac failure caused by being negatively inotropic.

169
Q

What are the side effects of Bendroflumethiazide?

A
  • Hypovolaemia
  • Hypotension
  • Reduced –> K, Na, Mg, Ca
  • Hyperuricaemia –> Gout
  • Erectile dysfunction
170
Q

What will 1 tablet of atenolol reduce your mmHg?

171
Q

What is heart failure?

A

A complex clinical syndrome of signs and symptoms that imply that the hearts ability of acting as a pump is compromised.

172
Q

What is the most common cause of HF?

173
Q

What hormones do the heart produce?

A

The heart produces ANP and BNP

174
Q

What are ANP and BNP metabolised by?

175
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
176
Q

How can NEP inhibitors work in heart failure?

A
  1. NEP metabolises ANP and BNP

2. NEP inhibitors can increase the level of ANP +BNP in serum

177
Q

What is the counter-regulatory system to RAAS?

A

ANP/BNP hormones

178
Q

What nitrates are used in Heart failure?

A

Isosorbide mononitrate

GTN spray

179
Q

What are the side effects of nitrates?

A

Headaches, syncope and tolerance

180
Q

Why are women less likely to develop heart failure?

A

Oestrogen is a protective hormone.

181
Q

What is the different compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation and hypertrophy
182
Q

How does the sympathetic system compensate for heart failure?

A

Improves ventricular function by increasing HR and contractility = CO maintained

Causes arteriolar constriction which increases after load and myocardial work

183
Q

How does the RAAS system compensate for heart failure?

A

Reduced CO leads to reduced renal perfusion so it activates RAAS –> more fluid + preload

Causes arteriolar constriction which increases afterload and myocardial work

184
Q

How do Natriuretic peptides compensate for heart failure?

A
  • Diuretic
  • Hypotensive
  • Vasodilators
185
Q

What are the signs of left side heart failure?

A
  1. Pulmonary crackles
  2. Added heart sounds (3rd and 4th) and murmurs
  3. Displaced apex beat
  4. Tachycardia
186
Q

What are the causes of Heart failure?

A
  • Ischaemic heart disease
  • Hypertension
  • Alcohol excess
  • Cardiomyopathy
  • Valvular
  • Endocardial and pericardial causes
187
Q

What is the pathophysiology of Heart failure?

A

When the HF, compensatory mechanisms attempt to maintain CO

As HF progresses, mechanisms are exhausted and become pathophysiological

188
Q

What are the symptoms of Heart failure?

A
  • Breathlessness and Tiredness/fatigue

- Swelling in hands ankles and feet – peripheral oedema

189
Q

What are the broad categories of Heart failure?

A

Systolic failure – ability of the heart to pump blood around the body is impaired

Diastolic failure – the heart is pumping blood effectively but relaxing and filling abnormally

190
Q

What investigations would you do in someone with Heart failure?

A
  1. ECG
  2. CXR – cardiac enlargement
  3. Natriuretic peptide levels – rise indicates HF

If suspected HF, patient should have an echocardiogram

191
Q

What is the management of Heart failure?

A

First line – vasodilator therapy (ACEi, beta blockers) via the neurohumoral blockade (RAAS-SNS)
- Perindopril

Beta blockers in HF – Metoprolol, bisoprolol, carvedilol and Nebivolol

Drugs for symptom relief

Diuretics –> thiazides (Bendroflumethiazide) and loop diuretics –> Na loss + H20 loss

192
Q

What are the two stages of hypertension?

A

Stage 1 – 140/90 and 135/85

Stage 2 – 160/100 and 150/95

193
Q

How would you diagnose hypertension?

A

Offered ambulatory blood pressure monitoring (ABPM) to confirm diagnosis)

Suspected hypertension – 140/90mmHg or higher

194
Q

What is the equation for blood pressure?

195
Q

What are the functions of angiotensin 2?

A
  1. Vasoconstrictor
  2. Activates sympathetic nervous system  Increased NAd
  3. Activates aldosterone = Na+ retention
  4. Vascular growth, hyperplasia and hypertrophy
196
Q

How does the sympathetic nervous system increase BP?

A
  • Noradrenaline is a vasoconstrictor  increased TPR
  • NAd has positive chronotropic + inotropic effects
  • It causes increase renin release
197
Q

What are 3 examples of ACEi?

A
  1. Ramipril
  2. Enalapril
  3. Perindopril
198
Q

Where are ACEi clinically indicated in?

A

Hypertension, heart failure and diabetic neuropathy

199
Q

What are the side effects of ACEi?

A
  • Hypotension
  • Hyperkalaemia
  • Acute renal failure
  • Teratogenic
200
Q

What can cause increased kinin production?

201
Q

How does ACE increase kinin production?

A
  • ACE converts bradykinin into inactive peptides

- Therefore ACE inhibitors lead to a build up of kinin

202
Q

What is the side effect of increased kinin?

A

Dry chronic cough, Rash, anaphylactoid reaction

203
Q

When are ARBs used?

A

When ACEi are contraindicated

204
Q

What are ARBs?

A

Angiotensin 2 receptor blockers

205
Q

What receptor does ARBs work at?

A

AT-1 receptors

206
Q

What are 3 examples of ARBs?

A

Candesartan, valsartan, losartan

207
Q

When are ARBs used?

A

Indicated in hypertension, heart failure and diabetic neuropathy

208
Q

What are calcium channel blockers?

A

L type Ca2+ channels

209
Q

Give 4 types of Calcium channel blockers

A
  1. Amlodipine
  2. Felodipine
  3. Diltiazem – acts on heart and vasculature
  4. Verapamil – acts primarily on the heart
210
Q

What are dihydropyridines?

A

A class of CCB –> arterial vasodilators –> Amlodipine and felodipine

211
Q

When are dihydropyridines indicated in?

A

Hypertension, IHD, Arrhythmia

212
Q

What are the potential side effects of CCBs due to vasodilation?

A
  • Flushing
  • Headache
  • Oedema
213
Q

What is a potential side effect of CCBs due to their negatively inotropic nature?

A

Worsening heart failure

214
Q

What is a potential side effect of CCBs due to their negatively chronotropic nature?

A

Bradycardia

AV block

215
Q

What are the side effects of verapamil?

A
  • Worsening Cardiac failure
  • Bradycardia
  • Atrioventricular block
  • Constipation
216
Q

A patient on CCBs comes in with constipation, which CCB might they be on?

217
Q

What are 3 examples of beta blockers?

A
  1. Bisoprolol (Beta 1 selective)
  2. Atenolol
  3. Propanolol (Beta ½ non selective)
218
Q

What conditions are beta blockers clinically indicated in?

A
  1. IHD
  2. Heart failure
  3. Arrhythmia
  4. Hypertension
219
Q

What are the side effects of beta blockers?

A
  1. Fatigue.
  2. Headache.
  3. Nightmares.
  4. Bradycardia.
  5. Hypotension.
  6. Cold peripheries.
  7. Erectile dysfunction.
  8. Bronchospasm.
220
Q

What is an example of a thiazide ?

A

thiazide Bendroflumethiazide

221
Q

What do thiazides work on?

A

Distal tubule in the kidney

222
Q

Give two examples of loop diuretics

A
  1. Furosemide

2. Bumetanide

223
Q

What is a K sparing diuretic?

A

Spironolactone

224
Q

Why is spironolactone particularly effective?

A

Has anti-aldosterone effects too

225
Q

When are diuretics clinically indicated?

A

HF and hypertension

226
Q

What are the side effects of diuretics?

A
  1. Hypovolaemia
  2. Hypotension
  3. Reduced Serum Na, K , Mg, Ca
  4. Increased uric acid  gout
  5. ED
  6. Impaired glucose tolerance
227
Q

You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?

A

Calcium channel blockers (as this patient is over 55) e.g. amlodipine.

228
Q

You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn’t controlled. What would you do next for this patient?

A

You would combine ACE inhibitors or ARB with calcium channel blockers.

229
Q

You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?

A

You would combine the ACEi/ARB and calcium channel blockers with a thiazide diuretic e.g. bendroflumethiazide.

230
Q

What is the vaughan williams classification?

A

Used to group anti-arrhythmic drugs

231
Q

What are VW class 1 drugs?

A

Class 1 – Na channel blockers. 3 Sub divisions

1a. Disopyramide
1b. Lidocaine
1c. Flecainide

232
Q

What are VW class 2 drugs?

A

Class 2 – Beta blockers

2a. propranolol
2b. atenolol
2c. bisoprolol

233
Q

What are VW class 3 drugs?

A

prolong action potential e.g. amiodarone

234
Q

What are VW class 4 drugs?

A

Class 4 drugs – CCB but not dihydropyridines as they don’t affect the heart

  1. Verapamil
  2. Diltiazem
235
Q

What is Digoxin?

A

Inhibits Na/K pump therefore making AP more positive and ACh is released from PS nerves.

236
Q

What are the main affects of Digoxin?

A
  • Bradycardia
  • Reduced atrioventricular contraction
  • Increased force of contraction (positive inotrope)
237
Q

Where is Digoxin clinically indicated?

238
Q

What are the side effects of Digoxin?

A

Nausea, vomiting, diarrhoea, confusion

239
Q

What are two drugs that increase the QT interval?

A
  1. Sotalol

2. Amiodarone

240
Q

What are the side effects of drugs that increase the QT intervals?

A
  1. Pro-arrhythmic effects.
  2. Interstitial pneumonitis.
  3. Abnormal liver function.
  4. Hyper/hypothyroidism.
  5. Sun sensitivity.
  6. Grey skin discolouration.
  7. Corneal micro-deposits.
  8. Optic neuropathy
241
Q

What can you use Na channel blockers in and how do they work?

A

Ventricular tachycardia – block inactivation of Na Channel

242
Q

What is the most useful beta blocker to control arrythmias?

A

Propranolol

243
Q

What does Furosemide block?

A

Na/K/2Cl- transporter

244
Q

How do beta blockers prevent symptom relief in angina?

A
  • Reduce O2 demand – neg chronotropic (HR)
  • Reduce O2 demand – neg inotropic (Contractility)
  • Increase O2 distribution by slowing HR
245
Q

Why can Doxazosin be used in hypertension?

A

Alpha 1 receptor antagonist.

246
Q

ECG - What is the J joint?

A

Where the QRS complex becomes the ST segment

247
Q

What is the normal axis of a QRS complex?

A

-30 degrees to 90 degrees

248
Q

ECG - What does the P wave represent?

A

Atrial depolarisation

249
Q

ECG - how long should a PR interval be?

250
Q

What might a long PR interval indicate?

A

Heart block

251
Q

How long should a QT interval be?

252
Q

ECG - what deos the QRS complex represent?

A

Ventricular depolarisation

253
Q

ECG - what does the T wave represent?

A

Ventricular repolarisation

254
Q

ECG - Where would you place lead 1?

A

Right arm to Left arm with positive electrode being at the left arm at 0 degrees.

255
Q

ECG - Where would you place lead 2?

A

Right arm to left leg with positive electrode being at the left leg at 60 degrees.

256
Q

ECG - Where would you place lead 3?

A

Left arm to left leg with positive electrode being at left leg at 120 degrees

257
Q

Where would you place avF?

A

From halfway between left arm and right arm to the left leg with the positive at the left leg at 90 degrees

258
Q

Where would you place avL?

A

From halfway between right arm and left leg to the positive electrode on the left arm at -30 degrees.

259
Q

Where would you place avR?

A

From halfway between left arm and left leg to the right arm with positive electrode at the right arm at -150 degrees.

260
Q

What is the dominant pacemaker of the heart?

261
Q

How many seconds do the small and large squares represent on ECG paper?

A 
Small = 0.04s 
Large = 0.2s
262
Q

How long should a QRS complex be?

A

Less than 110 ms

263
Q

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

264
Q

in which lead are all waves negative?

265
Q

In which leads must the R wave grow?

A

Chest leads V1 to V4

266
Q

In which leads must the S wave grow?

A

Chest leads V1 to V3 then dissapear in V6.

267
Q

In which leads should T waves and P waves be upright?

A

Leasd 1,2 and V2–>V6

268
Q

What may tall pointed P waves on an ecg suggest?

A

Right atrial enlargement

269
Q

What may M shaped P waves on an ecg suggest?

A

Left atrial enlargement

270
Q

What are 3 signs of abnormal T waves?

A

Symmetrical
Tall and peaked
Biphasic or inverted

271
Q

What happens to the QT interval when the HR decreases?

A

QT interval decreases

272
Q

Which part of the ecg does the plateau phase of the cardiac action potential coincide with?

A

QT interval

273
Q

Define Shock

A

When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.

274
Q

Give 3 signs and symptoms of shock?

A 
Pale
Sweaty
Cold
Pulse is weak but rapid 
Reduced urine output 
Confusion
Weakness/collapse
275
Q

What can cause hypovolaemic shock?

A

Loss of blood

Loss of fluid

276
Q

Describe the vital signs in type 1 shock e.g. blood loss, bp, pulse presure , RR and urine output.

A 
15% blood loss 
100bpm +
normal pulse and bp 
resp rate 14-20 
Urine output 30ml/h
277
Q

Describe the vital signs in type 2 shock e.g. e.g. blood loss, bp, pulse presure , RR and urine output.

A 
15-30% blood loss 
100bpm+ 
normal bp 
decreased pulse
RR - 20-30 
Urine output 20-30ml/h
278
Q

Describe the vital signs in type 3 shock e.g. e.g. blood loss, bp, pulse presure , RR and urine output.

A 
30-40% blood loss
120bpm 
blood pressure and pulse down 
RR - 30-40 
Urine output 5-15ml/hr
279
Q

What can cause cardiogenic shock?

A

Cardiac tamponade
PE
MI
Fluid overload

280
Q

What is septic shock?

A

A systemic inflammatory response associated with an infection (Bacterial endotoxins)

281
Q

What is anaphylactic shock?

A

An intense allergic reaction associated with massive histamine release and haemodynamic collapse.

282
Q

What is the treatment for anaphylactic shock?

A

Adrenaline and supportive therapy

283
Q

Give 2 signs of Acute resp distress syndrome?

A

Imapried oxygenation
No cardiac failure
Bilateral pulmonary infiltrates

284
Q

Describe the pathophysiology of ARDS?

A
  1. Exudative phase –> increased vasc permeability leads to platelet, fibrin and clotting factor exudate
  2. Proliferative phase - fibroblast proliferation
  3. Fibrotic phase
285
Q

Give 4 extra-pulmonary causes of ARDS?

A 
Sepsis
Trauma
Shock 
Drug reaction
Pancreatitis
286
Q

Give 3 pulmonary causes of ARDS?

A

Pneumonia
Near drowning
Smoke inhaling

287
Q

How much serous fluid is there between the visceral and parietal pericardium?

288
Q

What is the function of the serous fluid?

A

Acts as a lubricant so smooth movement of the heart inside the pericardium.

289
Q

What is the function of the pericardium?

A

Restrains the filling volume of the heart

290
Q

Name 3 Cardiomyopathies

A
  1. Hypertrophic (HCM)
  2. Dilated (DCM)
  3. Arrhythmogenic R/L ventricular
291
Q

What is the cause of HCM?

A

Sarcomeric gene mutations e.g. beta myosin and troponin T –> Affects 1 in 500

292
Q

What is the cause of ARVC/ALVC?

A

Desmosome gene mutations

293
Q

What is the inheritance pattern of CMs?

A

Cardiomyopathies tend to be AD –> offspring have a 50% chance of getting infected

294
Q

What is the pathophysiology of HCM?

A

Systole is normal but diastole is affected

Heart is unable to relax due to the thickening of ventricular walls

295
Q

What is the pathophysiology of DCM?

A

Ventricular dilation and dysfunction = poor contractility

296
Q

What is the pathophysiology of ARVC/ALVC?

A

Desmosomes attach cells via intermediate filaments

Desmosome mutations lead to myocytes being pulled apart

Ventricles are replaced with fatty fibrous tissues

297
Q

What is the symptoms of HCM?

A

Angina, Dyspnoea and syncope

298
Q

What is the symptoms of DCM?

A

Similar to HF –> breathlessness, tiredness and oedema

299
Q

What is a sign of ARVC/ALVC?

A

Ventricular tachycardia

300
Q

What would an ECG look like in a patient with HCM?

A

Large QRS complex and large inverted T waves.

301
Q

What might an ECG look like from a person with ARVC/ALVC?

A

Epsilon waves

302
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts diastole

303
Q

What is the cause of restrictive cardiomyopathy?

A

Amyloidosis –> deposition of amyloid.

304
Q

What are channelopathies?

A

Mutations in genes coding for ion channels.

Common symptom is syncope

305
Q

Give 3 examples of channelopathies

A

Long QT syndrome
Short QT syndrome
Brugada - Na defect with St elevation
CPVT

306
Q

What are 4 main features of tetrology of fallot?

A
  • Ventricular septal defect
  • Overriding aorta
  • RV hypertrophy
  • Pulmonary stenosis
307
Q

Is a baby cyanotic in TOF?

A

greater pressure in RV then LV so blood is shunted into LV

308
Q

What is VSD?

A

Abnormal connection between 2 ventricles

309
Q

Would a baby be cyanotic with VSD?

A

Would not be cyanotic –> higher pressure in the LV than RV so blood shunted to RV

310
Q

What are the clinical science of VSD?

A
  • High Pulmonary blood flow
  • Breathless poor feeding and failure to thrive
  • Tachycardia
  • Increased RR
311
Q

What is ASD?

A

Abnormal connection between the two atria

312
Q

What is the signs of a large ASD?

A
  1. Enlarged pulmonary arteries
  2. Right heart dilation
  3. SOBOE
  4. Increased chest infection
  5. Significant increase in blood flow through the right heart and lungs – pulmonary flow murmur
313
Q

Would a baby be cyanotic with ASD?

A

Would not be cyanotic –> Higher pressure in LA than RA so blood is shunted L to R so more blood to the lungs –> No cyanosis

314
Q

What is ASVD?

A

Atrioventricular septal defect (hole in centre of heart)

315
Q

What are the signs of ASVD?

A
  • Breathlessness

- Poor feeding and poor weight gain

316
Q

What is a PDA?

A

Patent ductus arteriosus

317
Q

What are the signs of a PDA?

A
  1. Torrential flow from aorta to the pulmonary arteries –> pulmonary hypertension
  2. Breathlessness
  3. Poor feeding, failure to thrive
  4. Risk of endocarditis
318
Q

What controls the sinus node discharge rate?

A

Autonomic nervous system

319
Q

Define sinus rhythm

A

A p wave that precedes each QRS complex.

320
Q

Give 3 consequences of arrhythmia

A 
Sudden death
syncope
Dizziness 
Palpitations 
Asymptomatic
321
Q

Give two categories of tachycardia

A

Supra-ventricular tachycardia

Ventricular tachycardia

322
Q

Where does supra-ventricular tachycardia arise from?

A

From the atria or the atrio-ventricular junction.

323
Q

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

324
Q

Where does ventricular tachycardia arise from?

A

Ventricles

325
Q

Do ventricular tachycardias have narrow or broad QRS complexes?

326
Q

Name 3 Supra-ventricular tachycardias.

A 
AF
Atrial flutter
Focal atrial tachycardia 
AV node re-entry tachycardia 
Accessory pathway
327
Q

Give 4 causes of sinus tachycardia

A 
Physiology response to excercise
Anaemia 
Fever
HF
Hypovol
328
Q

Describe 2 characteristics of an ECG with someone with Atrial fibrilation

A
  1. Absent P waves
  2. Fine oscillation of the baseline

This is because the aV node and ventricles can’t keep up with the atria –> irregulary irregular pulse

329
Q

Give 4 symptoms of AF

A 
Palpitations
Sob
Fatigue
Chest pain 
Increased risk of thromboembolism
330
Q

What score can be used to calculate the risk of stroke in somone with AF?

A

CHADS2 VASc

331
Q

What does the CHADS2 VASc score take into account?

A 
Age
Hypertension
Previous stroke/TIA
Diabetes
Female

Over 2 = need for anti coag

332
Q

What is the treatment for AF?

A
  1. Rate control - BB, CCB an digoxin
  2. pacemaker or flecainide
  3. Long term catheter ablation and pacemaker
333
Q

What would the ECG be like in a pt with atrial flutter?

A

Narrow QRS

Sawtooth flutter waves

334
Q

What pathophysiological mechanism can cause atrial flutter?

A

Re-entry mechanism - blockage of normal circuit –> another pathway forms and takes a different course and renters the circuit causing tachycardia.

335
Q

What is the commonest type of supraventricular tachycardia?

A

AV node re-entry tachycardia.

P waves are seen within the QRS complex

336
Q

Give 4 symptoms of AVNRT

A 
Tachycardia
Sudden/onset palpitations 
SOB
Chest pain 
neck pulsation
337
Q

Describe the acute treatment of AVNRT

A

Vagal manoeuvere and adenosine

BB,CCB and Flecainide will be given to prevent future episodes.

338
Q

What is the pathophysiology of accessory pathway arrythmias?

A

Congenital muscle strands connect atria and ventricles –> causing pre excitation of the ventricles.

339
Q

Describe 3 ECG features in someone with accessory pathway arrythmia

A
  1. Delta wave
  2. Short PR interval
  3. Slurred QRS complex
340
Q

Describe the pathophysiology of focal atrial tachycardia

A

Another area of the atrium becomes more autonomic than the sinus node so sinus node function is taken over

ECG –> Abnormal P waves before a normal QRS

341
Q

What is the urgent treatment for Ventricular tachycardia?

A

DC cardioversion.

Long term an implantable defibrilator would be inserted

342
Q

Give 3 causes of long QT syndrome?

A

Congenital
Electrolyte disturbances –> hypo cal and hypo kal
Drugs

343
Q

Give 2 signs of long QT syndrome?

A

Palpitations

Syncope

344
Q

Give 4 causes of sinus bradycardia?

A

Ischaemia
Fibrosis of atrium
Inflammation
Drugs

345
Q

Give 3 causes of Heart block?

A

CAD
Cardiomyopathy
Fibrosis

346
Q

What heart block is assocated with wide QRS in an abnormal pattern?

A

RBBB or LBBB

Phase 2a Sheffield Medicine (10 decks)

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