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Cardiovascular System > Stroke, atherosclerosis, oedema, arrhythmias and valve disease > Flashcards

Stroke, atherosclerosis, oedema, arrhythmias and valve disease Flashcards

1
Q

Define red and white thrombi (origin and composition)

A
  • Red thrombus: contains mostly RBCs and fibrin. Venous origin, caused by stasis or hypercoagulability
  • White thrombus: contains lipids/platelets and fibrin. Arterial origin, broken off atheroma plaque
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2
Q

What are the three components of Virchow’s triad?

A
  • Change in blood flow (ie stasis)
  • change in blood components (ie hypercoagulability)
  • change in blood vessel (ie endothelial damage)
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3
Q

What investigations should be done to diagnose pulmonary embolism?

A
  • If Wells probability score low - do a blood test for D-Dimer
  • If Wells probability score high - do CT Pulmonary Angiogram
    If D-Dimer positive - do CT Pulmonary Angiogram
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4
Q

What are the two main types of Venous Thromboembolism (VTE)?

A

Deep vein thrombosis (DVT) and Pulmonary Embolism (PE)

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5
Q

Define embolism

A

Material in the circulation which dislodges from original place and moves to another area of the body. Can be a blood clot but also air, lipids etc

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6
Q

What are two causes for stasis (blood pooling, change in blood flow in Virchow’s triangle)?

A

Long flights, immobility/bedbound status

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7
Q

What can cause hypercoagulability?

A

Inherited or acquired (Pregnancy, surgery, cancer)

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8
Q

What can cause endothelial damage?

A 
Endothelial dysfunction (caused by smoking, hypertension, hypercholesterolaemia) 
Endothelial injury (IV catheters, trauma, surgery)
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9
Q

What are common signs of DVT?

A

Unilateral swelling, discomfort, redness, may be silent

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10
Q

Define claudication

A

Pain in leg(s) due to ischaemia caused by occluded artery supplying the leg.

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11
Q

What is a common complication of DVT and what are its implications?

A

Post-thrombotic syndrome, can affect up to half the patients who have had DVT in previous months.
Causes chronic pain, swelling, redness, ulcers and damage to valves in the veins

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12
Q

How is DVT diagnosed?

A
  1. Clinical assessment and Wells score
  2. Wells test result low –> blood test for D-Dimer
  3. Wells test high/D-Dimer positive –> compression ultrasound or doppler ultrasound
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13
Q

What is the Wells probability test?

A

It’s a measure to calculate the risk of thrombosis based on risk factors

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14
Q

What is a D-Dimer?

A

It’s a byproduct of the breakdown of cross-linked fibrin following fibrinolysis

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15
Q

What are the diagnostic advantages and disadvantages of D-Dimer blood testing?

A

It’s very sensitive to D-Dimer presence in the blood, so useful to rule out thrombosis.
It’s not very specific, there are other causes for raised D-Dimer levels so a positive result may not be due to thrombosis

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16
Q

What are the four main types of valve disease?

A

Mitral stenosis,
Mitral regurgitation,
Aortic stenosis
Aortic regurgitation

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17
Q

Which heart valves are more likely to have congenital abnormalities?

A

Right heart valves - tricuspid and pulmonary

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18
Q

What are the main causes of mitral stenosis?

A 
Rheumatic heart disease 
Systemic diseases (SLE, RA)
Congenital defect
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19
Q

What are the main symptoms of mitral stenosis?

A 
Shortness of breath (exertion)
Shortness of breath (pulmonary oedema)
Haemoptysis
Hoarse voice (compressed recurrent laryngeal nerve)
Infective Endocarditis
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20
Q

What are the main signs of mitral stenosis?

A 
Mitral facies
RV hypertrophy 
Pulmonary oedema
Pulmonary hypertension
Raised JVP (a wave)
Tapping apex beat 
Diastolic thrill
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21
Q

Which valve diseases have a long asymptomatic phase?

A

Aortic stenosis and aortic regurgitation

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22
Q

What investigations can be done to diagnose mitral stenosis?

A 
Cardiac catheter
CXR
ECG
Echocardiogram 
Cardiac magnetic resonance
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23
Q

What are the steps in diagnosing Pulmonary Embolism?

A

Wells score low - D-Dimer
D-Dimer positive - CT Pulmonary Angiogram, V/Q scan
Wells score high - CT Pulmonary Angiogram, V/Q scan

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24
Q

What are the common signs and symptoms of PE?

A

Pleuritic chest pain, SOB, tachycardia, haemoptysis, pleural rub
If PE severe: severe SOB, central cyanosis, low BP, raised JVP, sudden death

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25
Q

What are the main treatment options for Vascular Thromboembolism (VTE)?

A

Anticoagulants (fractionated or LMW heparin; warfarin, DOACs)
Thrombolysis (eg alteplase, in severe cases)

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26
Q

What measures can be taken to prevent VTE occurring?

A

Early mobilisation, stockings, mechanical or pharmaceutical thromboprophylaxis

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27
Q

What are the main aims of VTE treatment?

A

Prevent recurrence, prevent clot extension and further embolisation

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28
Q

What is a possible long term complication of PE?

A

Pulmonary hypertension

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29
Q

How can PE lead to pulmonary infarction, and how likely is it?

A

Infarction rare due to collateral circulation in lungs.

It occurs through leaking fluid into alveoli due to increased pressure in bronchial circulation

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30
Q

What are three important considerations when VTE has been diagnosed?

A
  • Clear cause of VTE (eg recent surgery, long flight)
  • Signs or symptoms indicating underlying malignancy
  • Chance of recurrence
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31
Q

What are the common causes of abdominal aortic aneurysms?

A
  • Atherosclerosic disease
  • Connective tissue diseases (eg Marfan’s Syndrome)
  • Infection
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32
Q

What are common risk factors for aneurysms?

A

Same ones as for atheromatous plaques:

Hypertension, age, smoking, diabetes, family history, high cholesterol, males

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33
Q

When should surgical repair of aneurysm be considered?

A

If aneurysm is enlarged to >5.5cm

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34
Q

What are the most common presentations of aneurysm?

A

Nothing, it’s normally picked up incidentally (especially through ultrasounds for gallstones). May present as back pain

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35
Q

What is the purpose of screening for aneurysms?

A

It helps to identify aneurysms before they rupture and monitor ones which are not large enough to call for repair

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36
Q

If an abdominal aortic aneurysm measuring 3-4.5cm is found, what is the course of action?

A

Patient should be discharged an be invited back for yearly ultrasound scans to monitor the aneurysm

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37
Q

If an abdominal aortic aneurysm measuring 4.5-5.5cm is found, what is the course of action?

A

Patient should be discharged and be invited back every 3 months for a surveillance ultrasound scan

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38
Q

What are common presentations of a ruptured abdominal aortic aneurysm?

A

Shock
back/side/abdominal pain
haematodynamic instability
hypoperfusion

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39
Q

What are some less common presentations of a ruptured abdominal aortic aneurysm?

A 
Distal embolisation (toes, kidneys, colon)
compression of duodenum
compression of ureter
aortocaval fistula
aortoenteric fistula
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40
Q

What are the surgical repair options for a ruptured abdominal aortic aneurysm?

A

Open repair or endovascular repair (EVAR)

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41
Q

What imaging techniques are used for assessing abdominal aortic aneurysm size, and what are their pros and cons?

A

Ultrasound:
Pros: cheap, accessible, tolerated by patient
Cons: operator dependent, no anatomic detail

CTA/MRA scan:
Pros: very quick (30s), not operator dependent, very clear anatomic image
Cons: radiation and contrast

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42
Q

What factors should be considered when assessing surgical repair for abdominal aortic aneurysm?

A

Patient fitness (lung, heart, kidney function)
Patient wishes
Aneurysm size
Anatomy (determines which type of surgery is suitable)

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43
Q

What are three main treatment options for abdominal aortic aneurysms?

A

Conservative treatment
Endovascular repair (EVAR)
Open repair

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44
Q

List some of the complications of open repair for abdominal aortic aneurysms

A

Pain/scarring/bleeding/dehiscence/wound infection
Damage to structures adjacent to aorta (nerves, bowel, veins, ureter)
distal embolisations and ischaemia, graft infection
colon ischaemia (redundant inferior mesenteric artery), kidney damage,
CVA/MI/PE

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45
Q

List some of the complications of EVAR for abdominal aortic aneurysms

A 
Pain/scar/bleeding/wound infection
Endoleak
Damage to endothelium (femoral dissection, pseudoaneurysm)
distal embolisations, graft infection, 
CVA/MI/PE
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46
Q

What is an endoleak?

A

It’s blood leakage in the area of the aneurysm that has been grafted

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47
Q

What investigation should be done to assess whether an aneurysm rupture should be repaired with open repair or EVAR?

A

CT scan to assess anatomic suitability for EVAR

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48
Q

When is an endarterectomy performed?

A

When a patient has/has had TIA/stroke symptoms and the relevant carotid artery is >70% but <99% occluded

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49
Q

What course of action should be taken if one carotid artery is completely occluded?

A

Best medical care (BMC), operation will not benefit patient since other arteries are still supplying Circle of Willis

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50
Q

What investigations should be done when a patient presents with a stroke?

A

CT scan - rule out a haemorrhagic stroke

Doppler ultrasound - to assess degree of carotid stenosis

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51
Q

What is the main management aim of TIA/stroke, and what are the common management steps?

A

Management to reduce risk factors:

  • smoking cessation
  • antiplatelet (2x for first 3 months)
  • statin
  • blood pressure medication
  • diabetic control
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52
Q

What investigations should be carried out to diagnose stroke/TIA?

A 
History
examination
bloods (FBC, lipids)
ECG (24hr)
CT/MRI
carotid ultrasound scans
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53
Q

What are the possible complications of an endarterectomy?

A

Bleeding, scarring, pain, infection
anaesthetic complications
damage to recurrent laryngeal nerve
perioperative stroke (thrombosis, hypoperfusion)

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54
Q

What factors can influence the management decision for stroke? (ie endarterectomy or best medical treatment)?

A 
Patient wishes
Anatomic suitability
Degree of carotid stenosis
Time since stroke/TIA 
Females
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55
Q

When is the most beneficial time to carry out endarterectomy to reduce further events?

A

First 2 weeks post event (faster is better in women)

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56
Q

When would carotid stenting be considered in the prevention of stroke?

A

If patient is not anatomically suitable for endarterectomy (eg scarring or occlusion is further up the internal carotid artery)

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57
Q

What treatment will be offered to a symptomatic patient with 60% carotid stenosis, and to one with 75% carotid stenosis?

A

60% - best medical treatment only

75% - best medical treatment + endarterectomy (or stenting if anatomically unsuitable for endarterectomy)

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58
Q

What are the four main types of ischaemic stroke?

A

Total Anterior Circulation Stroke (TACS)
Partial Anterior Circulation Stroke (PACS)
Lacunar Stroke (LACS)
Posterior Circulation Stroke (POCS)

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59
Q

What is POCS most likely to present with?

A 
visual disturbance (Homonymous hemianopia)
breathing problems
tinnitus
Horner's syndrome
loss of function/sensation
coma
dizzyness
balance problems
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60
Q

What is TACS most likely to present with?

A

Symptoms include face/arm/leg weakness and loss of sensation, speech disturbance, loss of vision

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61
Q

What is PACS most likely to present with?

A

Combination of 2/3 of the symptoms seen in TACS. Restricted hemiparesis/loss of sensation only, or speech/motor function disturbance only

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62
Q

What is LACS most likely to present with?

A

Depends on the location.

Sensory only/motor only/sensorymotor/ataxic hemiparesis

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63
Q

What are the two main presentations of stroke and their prevalence?

A 
Ischaemic stroke (85%)
Hemorrhagic stroke (15%)
64
Q

Which type of stroke may go unnoticed and undiagnosed?

A

LACS

65
Q

List some of the risk factors for stroke

A 
Atrial Fibrillation
Smoking
Hypertension 
Diabetes
Previous stroke/MI
Hypertension
Hypercholesterolaemia
Race
Family history
Age
Gender
66
Q

What are the 5 main presenting characteristics of a stroke?

A 
Loss of function
Loss of sensation
Loss of vision
Loss of balance
Loss of speech
67
Q

What is the main cardiovascular cause for cardioembolic stroke?

A

Atrial Fibrillation

68
Q

What is the main cardiovascular cause for haemorrhagic stroke?

A

Hypertension

69
Q

What are the benefits of stroke units?

A

Expertise
Specialised care
Early mobilisation
Attention to improving functions eg swallowing, speech and language, rehabilitation

70
Q

What is the benefit of informing A&E of stroke from ambulance?

A

Reducing time it takes to get patient into hospital, to CT and thrombolysed

71
Q

What imaging investigation should be done when a patient presents with a stroke?

A

CT to rule out haemorrhage. If ischaemic, thrombolyse (tPA)

72
Q

Why is it important to improve swallowing function in stroke patients?

A

To avoid choking or aspiration pneumonia

73
Q

What type of stroke shows up best on CT scan?

A

Haemorrhagic stroke

74
Q

What type of stroke shows up best on MRI scan?

A

Ischaemic stroke

75
Q

What is the main complication of thrombolysis?

A

Bleeding

76
Q

What seems to be the most effective way to treat a stroke in an emergency?

A

Thrombolysis + thrombectomy (clot retrieval) if ischaemic stroke

77
Q

What are the contraindications for thrombolysis?

A

Age (>80)
Recent bleeding
severe hypertension

78
Q

When should hemicraniectomy be considered?

A
  • Patient is <60yo
  • ischaemic MCA occlusion with cerebral oedema
  • <48hrs from onset
79
Q

What common antiplatelet drugs are used in secondary prevention of stroke?

A

Aspirin
Clopidogrel
Dipyridamole

80
Q

What main treatment should be used for stroke prevention in patients with AF?

A

Anticoagulants

  • warfarin
  • DOACs (apixaban, rivaroxaban)
81
Q

What is the main cause of atherosclerosis?

A

Hypercholesterolaemia

82
Q

What is atherosclerosis?

A

Formation of atheromatous plaques in areas of damaged endothelium

83
Q

What are atheromatous plaques made up of?

A

Inner mass of dead macrophages, cholesterol, lipids, calcium

Outer cap made up of collagen and fibrous tissue (stimulated by PDGF)

84
Q

What does complicated atheroma mean?

A

It’s a rupture of an atheromatous plaque, which causes inflammation/thrombosis

85
Q

What are the two types of supraventricular tachycardia?

A
  • AV node re-entral tachycardia (extra conduction in atrial tissue)
  • AV re-entral tachycardia (extra conduction from atrium to ventricle)
86
Q

What characterises first degree heart block?

A

Slow conduction from sinoatrial node - long PR interval

87
Q

What characterises second degree heart block?

A

Mobitz 1 - increasing delay in PR segment until one P wave doesn’t conduct signal to ventricle
Mobits 2 - no pattern, random P waves do not conduct signal to ventricle (no QRS)

88
Q

What characterises third degree heart block?

A

P waves have no association with the QRS waves, occur indepentently of eachother

89
Q

What is the difference between atrial flutter and atrial fibrillation on an ECG?

A

Atrial flutter - sawtooth

Atrial fibrillation - no P wave

90
Q

What does Wolff-Parkinson-White Syndrome look like on an ECG?

A

Delta wave (slurred upstroke QRS, wide at the bottom and narrowing at the top)

91
Q

How to tell supraventricular and ventricular tachycardia apart on an ECG?

A

Supraventricular tachycardia - narrow QRS

Ventricular tachycardia - broad QRS

92
Q

Define AV nodal re-rentrant and AV re-entrant supraventricular tachycardia

A
  • AV nodal re-rentrant supraventricular tachycardia: conduction signal goes round in circles around the AV node
  • AV re-entrant supraventricular tachycardia: conduction signal sent to ventricles but moves back to the atria through accessory conduction circuit
93
Q

What are supraventricular ectopic beats?

A

Beats which come in earlier than they should

94
Q

Define Torsades de Pointes

A

Polymorphic ventricular tachycardia

95
Q

What are the main aims of atrial fibrillation treatment?

A 
Heart rate control (beta blockers, rate limiting CCBs)
Rhythm control (drugs, cardioversion, RFA)
96
Q

When should an internal defibrillator be inserted?

A

If VF/VT not secondary to reversible cause
If VT continuous and causing syncope or significantly reducing QoL
If VT and LV failure

97
Q

When should a pacemaker be inserted?

A

If alternating LBBB and RBBB
If severe or at risk of severe bradycardia
If second or third degree heart block

98
Q

What investigations should be carried out to diagnose AF?

A 
24hr ECG
blood test (to exclude hyperthyroidism and electrolyte abnormality)
99
Q

Which valve diseases can have a long asymptomatic period?

A

Aortic stenosis and aortic regurgitation

100
Q

How do aortic stenosis and regurgitation affect the pulse on examination?

A

stenosis - rising pulse

regurgitation - collapsing pulse

101
Q

What are common causes of mitral stenosis?

A

Rheumatic heart disease
congenital
systemic diseases (SLE, RA)

102
Q

What are common symptoms of mitral stenosis?

A

Haemoptysis
SoB
Pulmonary oedema
Systemic emboli (eg stroke)

103
Q

What are useful investigations for diagnosing mitral stenosis?

A

Echocardiogram
Cardiac catheterisation (ie angiography)
Cardiac MRI
to a lesser extent: ECG, CXR

104
Q

What medical treatments should be used for mitral stenosis?

A

Anticoagulants for AF

Diuretics

105
Q

What are common acute and chronic symptoms of mitral regurgitation?

A

acute - cardiogenic shock, severe SoB

chronic - fatigue, SoB on exertion, PND

106
Q

What are the main investigations carried out for mitral regurgitation?

A

Echocardiogram (transthoracic/transesophageal)
cardiac MRI
CXR
ECG

107
Q

What are the medical treatment options for acute and chronic mitral regurgitation?

A

acute - medical emergency: dobutamine (for cardiogenic shock); sodium nitroprusside (vasodilator), keep patient alive until they can go to surgery
chronic - nothing proven effective

108
Q

What are the medical treatment options for acute and chronic aortic regurgitation?

A

acute - medical emergency: dobutamine (for cardiogenic shock); sodium nitroprusside (vasodilator), keep patient alive until they can go to surgery
chronic - vasodilators

109
Q

What are the medical treatment options for aortic stenosis?

A

None unless pt develops heart failure

110
Q

What are the common symptoms of aortic stenosis?

A

Chest pain
Blackouts
SoB

111
Q

Name two conditions which can lead to VT/VF

A

Brugada syndrome

long-QT syndrome

112
Q

What treatment is most successful in stopping supraventricular tachycardia (nodal re-entral or re-entral)?

A

Radiofrequency Ablation

113
Q

What are two potential causes for long QT syndrome?

A

genetic

acquired (eg drugs)

114
Q

What is the definition of congestion?

A

Excess blood in systemic vessels

115
Q

What is the definition of oedema?

A

Excess fluid in interstitial space

116
Q

What are the effects of congestive heart failure?

A

Left heart failure: pulmonary oedema

Right heart failure: central venous congestion + portal venous congestion

117
Q

What are the consequences of central venous congestion?

A

raised JVP
hepatomegaly (hepatic central venous congestion)
peripheral oedema

118
Q

What is the main process behind transudate oedema?

A

changes in hydrostatic pressure in capillaries

119
Q

What is the main process behind exudate oedema?

A

increased capillary permeability as reaction to inflammatory process

120
Q

What components of oedema can be used to characterise the underlying process, and how?

A

Transudate - few proteins, low gravity

Exudate - lots of proteins, high gravity

121
Q

What is the process underlying lymphoedema?

A

obstruction of lymphatic vessels

122
Q

What are some examples of congestion in clinical practice?

A

DVT
Liver congestion in cirrhosis
Congestive heart failure

123
Q

How does congestive heart failure arise, and what does it result in?

A

LV and/or RV not efficiently pumping blood out
LV - backlog and congestion in lungs = pulmonary oedema
RV - backlog and congestion in systemic veins and portal system = peripheral oedema and hepatomegaly

124
Q

What can cause portal circulation congestion, and what are some potential consequences?

A

Portal systemic shunts:

  • Oesophageal varices
  • Caput medusae
125
Q

How does LV failure cause oedema?

A

Reduced CO
Activation of RAAS
Increased water/salt retention
Fluid overload = oedema

126
Q

What are the main forces controlling fluid in the vessels, and how do they lead to oedema?

A
  • Hydrostatic forces: increased pressure in capillary due to congestion can force fluid out of vessel
  • Oncotic forces: lack of proteins drawing fluid back into capillary can cause fluid buildup outside the vessel
127
Q

How does lymphedema come about?

A

Blockage of lymphatic system at capillary bed

128
Q

What type of oedema is found in congestive heart failure, and which starling force is at play?

A

Transudate oedema

Hydrostatic force imbalance

129
Q

What are starling’s forces and what is their function?

A

Hydrostatic pressure and oncotic pressure

Keeps balance of fluid inside and outside capillary

130
Q

At which point in circulation is hydrostatic or oncotic pressure higher?

A

Arterial circulation - hydrostatic force

Venous - oncotic force

131
Q

What are the two mainly occurring types of haemorrhagic stroke and their prevalence?

A
  • Intracerebral haemorrhage (9%)

- Subarachnoid haemorrhage (6%)

132
Q

what are the two major ischemic heart conditions which call for CABG?

A
  • left main stem stenosis

- three vessel disease

133
Q

what is meant by three vessel disease?

A

obstruction of the RCA, LAD and Cx

134
Q

what is left main stem stenosis?

A

stenosis of the bifurcation of the LCA into LAD and Cx

135
Q

What are three main complications of CABG surgery?

A

cardiac tamponade
stroke
death

136
Q

what can be some complications of open heart surgery (sternotomy)?

A 
infection of the wound/wires
sternal dehiscence (two sides grind agaisnt eachother)
sternal malunion (sternal sutures come apart)
137
Q

what are the main vessels used as bypass grafts?

A

mammary arteries
radial artery
reversed saphenous vein

138
Q

which valve diseases are most commonly operated on, and when should surgery be carried out?

A

Aortic most common, then mitral
if valve disease severe
if there is large vegetations on valves
if renal function keeps dropping or fever persists

139
Q

what options of valve replacements can be used?

A 
pig valve (biological)
mechanical valve
140
Q

what are the benefits and disadvantages of the different types of replacement valves?

A

biological - less chance of infection; no warfarin; won’t last as long
mechanical - higher chance of infection; makes noise; will last a lifetime but also be on warfarin for life

141
Q

which two organisms are most likely to cause what severity of infective endocarditis?

A

strep viridans - subacute IE

staph aureus - acute IE

142
Q

what is a benefit of mitral valve repair over replacement?

A

it’s better to keep as much of the native valve as possible

143
Q

IE affecting which types of replacement valves is more and less likely to be cured by only antibiotics?

A

native replacement valve - 90% chance of cure with only antibiotics
prosthetic valve - 50% chance of cure with only antibiotics

144
Q

what is the classification of anti-arrhythmic drugs called, and how does it classify the drugs?

A

Vaughan Williams Classification
Class 1 - (1a,1b,1c): sodium blockers
Class 2 - beta blockers (reduce sympathetic activity)
Class 3 - potassium channel blocker (longer repolarisation)
Class 4 - calcium channel blockers (rate limiting)

145
Q

what are the possible side effects of digoxin?

A

yellow vision
brady/tachicardia
VF/VT
nausea and vomiting

146
Q

what are the main drugs used to treat atrial fibrillation?

A

beta blockers
class 1a sodium channel blockers (quinidine)
anticoagulants (warfarin or DOACs)

147
Q

when are drugs like flecainide and amiodarone used in arrythmias?

A

in serious SVT, VT or arrhythmias not responding to beta blockers

148
Q

what is the mechanism of action of digoxin and which patient population is likely to be on it?

A

positive inotrope, blocks ATPase pump

often given to elderly patients with kidney failure

149
Q

what is the effect of the various sodium channel blockers on cardiac action potentials?

A 
class 1a - longer AP, delay refractory period
class 1b - shorter AP, accelerate refractory period
class 1c - no effect on AP or refractory period, stronger sodium block
150
Q

how is digoxin toxicity treated?

A

by stopping digoxin and administering Digibind

151
Q

what are class 1b antiarrythmics used for?

A

severe VT and VF

152
Q

give an example of antiarrhythmic medication for each Vaughan Williams classification

A 
class 1a - quinidine
class 1b - lidocaine, phenytoin
class 1c - flecainide
class 2 - bisoprolol, atenolol
class 3 - amiodarone
class 4 - verapamil, diltiazem
153
Q

how can warfarin be counteracted and why?

A

with vitamin K
warfarin stops vitamin K activation (which helps production of clotting factors) –> administering vitamin K increases its levels in the blood

154
Q

what are possible side effects of warfarin?

A

bleeding

teratogenicity

155
Q

what is the effect of adenosine on paroxysmal ventricular tachycardia?

A

returns heart to sinus rhythm

Cardiovascular System (8 decks)

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