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4TH YEAR - CSIM2 > Vascular Medicine > Flashcards

Vascular Medicine Flashcards

1
Q

Describe the different manifestations of atherosclerosis in the body

A

Coronary arteries:

  • Angina (semi-occluded vessel)
  • MI (plaque rupture or complete occlusion)
  • Microvascular disease

Carotid arteries

  • Stroke
  • TIA

Renal arteries

  • CKD
  • Renovascular hypertension

Peripheral arteries

  • Peripheral exertional leg pain
  • Critical limb ischaemia
  • Acute limb ischaemia
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2
Q

What is the pathogenesis of atherosclerosis?

A
  1. LDL particles migrate to arteries and oxidise, forming a fatty layer
  2. This attracts monocytes which expand at the site to form foam cells
  3. Foam cells accumulate to form a plaque
  4. Smooth muscle cells move to the intimate and contribute to the formation of a fibrous cap
  5. Over time this narrows the lumen, leading to reduced blood flow
  6. The cap releases collagen and elastin causing the plaque to rupture
  7. When the plaque ruptures, thrombosis is triggered and clots form which further impede blood flow
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3
Q

At what age does atherosclerosis BEGIN and become PATHOGENIC?

A

It begins in the teens, but complications secondary to ischaemia and plaque rupture occur in later years.

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4
Q

What are the signs and symptoms of peripheral arterial disease?

A 
SYMPTOMS
Atypical, exertional leg pain
Intermittent claudication
SIGNS
Absent pulses, cold white legs, ulcers, atrophic skin
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5
Q

What is critical limb ischaemia?

A

PAD that has progressed to the extent that the patient experiences rest pain relieved by hanging the foot outside the bed, and ischaemic ulcers.

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6
Q

What is acute limb ischaemia?

A

Medical emergency due to sudden thrombosis, emboli, occlusion or trauma. Presents with the 6Ps:

  • Pallor
  • Pulselessness
  • Perishingly cold
  • Pain
  • Paralysis
  • Parasthesia
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7
Q

How is acute limb ischaemia managed?

A

Open surgery, angioplasty, thrombolysis, anticoagulation

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8
Q

How is PAD diagnosed?

A

ABPI - ratio of systolic BP at the ankle to the systolic BP at the brachial arteries
>1.30 = noncompresible (elderly, diabetes)
0.91-1.3 = normal
0.71-0.9 = mild (likely arterial)
0.41 - 0.70 = moderate
<0.40 = severe (rest pain - likely critical)

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9
Q

What is the 1st line imaging for PAD?

A

Colour duplex ISS

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10
Q

Name some cardiovascular risk factors

A
  • Smoking
  • Age
  • Hyperlipidemia
  • Hypertension
  • DM
  • Previous CVD
  • Ethnicity
  • Fam hx
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11
Q

What are the features of the metabolic syndrome?

A
  • Insulin resistance
  • Central obesity
  • Hypertension
  • Dyslipidemia
  • Impaired glucose tolerance
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12
Q

Describe typical angina chest pain

A

Central crushing chest pain (pressure like, gripping, discomfort, heavy etc) that radiates to the neck, jaw, epigastrium or arms, lasting a few minutes

Precipitated by exertion, emotion, eating etc or spontaneous (unstable angina)

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13
Q

What is the single biggest risk factor for having a recurrent stroke having had a single TIA?

A

Hypertension

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14
Q

What are the cardiac differentials for chest pain? How do you differentiate?

A
  • Angina – shorter duration
  • MI – Symptoms that are lasting longer than 15 mins, nausea, pale, etc.
  • Pericarditis – Pain that varies with respiration and position (worse if you sit up)
  • Aortic Dissection – tearing feeling, radiates to back.
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15
Q

What is the definition of hypertension?

A

BP greater than or equal to 140/90mmHg

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16
Q

What is the main cause of hypertension?

A

Essential HTN (80%) - complex interaction of genes and environment

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17
Q

List some causes of secondary hypertension:

a) renal
b) endocrine
c) vascular
d) drugs
e) miscallaenous

A

a) glomerulonephritis, PCKD, diabetes, renovascular disease
b) cushings, phaeochromocytoma, conn’s, diabetes, thyroid, acromegaly
c) CAD, renal artery stenosis, coarctation of aorta
d) alcohol, amphetamines, cocaine, COCP, cyclosporin, erythropoeitin, cold/flu remedies

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18
Q

What is the main underlying pathophysiology of secondary hypertension?

A
  • Reduced elasticity and compliance of large arteries, due to accelerated accumulation of arterial calcium and collagen and degradation of elastin
  • Defective sodium storage leading to retention
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19
Q

How do the kidneys normally respond to low blood pressure?

A

Low blood flow stimulates secretion of renin from juxtaglomerular cells, which activates the RAAS.

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20
Q

How does renovascular disease affect blood pressure?

A

Stenosis to the kidneys will activate the RAAS causing an increase in BP

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21
Q

How does glomerulonephritis affect blood pressure?

A

Chronic inflammation causes impaired sodium processing at the glomeruli, so salt and excess fluid build up, contributing to hypertension.

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22
Q

How does PCKD affect blood pressure?

A

Increased sympathetic activity causes inappropriate renin secretion and NO inhibition. It also causes abnormally large levels of catecholamines (due to decreased production of renalase, an enzyme which normally metabolises catecholamines)

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23
Q

What potent circulating vasodepressor are many patients with renal disease deficient in?

A

Medullipin - this would usually lower pp

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24
Q

Describe the development of salt sensitive hypertension

A
  1. Exposure to stimuli that causes renal vasoconstriction
  2. Renal injury caused by tubular ischemia, causing impaired sodium excretion
  3. Sodium excretion restored to equal intake at the expense of shift to higher systemic blood pressure
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25
Q

How does Conn’s syndrome affect blood pressure? What is the typical biochem?

A

Conns syndrome = primary hyperaldosteronism due to benign adenoma

Adenoma causes:

  • high aldosterone
  • low potassium
  • normal sodium
  • low renin.

This leads to sodium retention, increased sympathetic drive and endothelial dysfunction

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26
Q

What investigations should be done for someone with Conn’s?

A

Aldosterone:renin ratio

HRCT/MRI - image adrenals to look for tumour (diagnostic)

Adrenal vein sampling - sample left and right aldosterone levels, marked discrepancy suggests unilateral adenoma, treat with surgery.

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27
Q

How does Cushings syndrome affect blood pressure?

A

Excess cortisol binds to the aldosterone receptor, activating RAAD

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28
Q

What investigations should be done for someone with Cushing’s?

A

Urinary free 24h cortisol levels (initial)
Low dose/high dose dexamethasone suppression test
Measure ACTH (give metyrapone to distinguish between pituitary and ectopic)
MRI (diagnostic of pituitary tumour)

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29
Q

How does Pheochromocytoma affect blood pressure?

A

Adrenal catecholamine-secreting tumour - catecholamines increase HR, causing vasoconstriction and sodium retention, leading to postural hypotension and labile BP.

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30
Q

What are the symptoms of phaeochromocytoma?

A

Labile BP
Postural hypotension
Headache

Many asymptomatic

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31
Q

Which syndromes is phaeochromocytoma associated with?

A

Von Hipper Lindau syndrome

MEN 2

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32
Q

What investigations should be done for someone with pheochromocytoma?

A
  • Plasma free mets (diagnostic)

- Urinary catecholamines (less convenient

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33
Q

What is shuttle enzyme deficiency?

A

A condition causing ‘apparent aldosterone excess’

  • failure of conversion from cortisol to cortisone (which would usually deactivate it)
  • hypertension
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34
Q

Which enzyme is deficient in shuttle enzyme deficiency?

A

11B-HSD

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35
Q

What is Liddles syndrome?

A

Genetic disorder causing increased activity of epithelial sodium channel so it is constantly open
- kidney excretes more potassium but retains sodium and water

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36
Q

What are the clinical and biochemical features of Liddle’s syndrome?

A

CLINICAL - autosomal dominant, early onset HTN

BIOCHEM - low K, metabolic alkalosis, high bicarb, low aldosterone, high sodium

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37
Q

How is Liddle’s syndrome investigated and managed?

A

INVESTIGATION - Bloods, ABG, genetic testing

MANAGEMENT - amiloride

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38
Q

How does acromegaly affect blood pressure?

A

Chronic exposure to GH and IGF-1 causes RAAS activation.

Also, associated insulin resistance increases BP

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39
Q

What are the components of routine assessment of raised BP?

A
  • BP
  • Height/weight/BMI
  • Pulses (radio femoral delay = coarctation)
  • Kidneys (palpable = PCKD)
  • End organ damage (U&E, creatinine, ECG)
  • Fundoscopy
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40
Q

What is the indication for ambulatory blood pressure monitoring?

A

Clinic BP 140/90 or higher

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41
Q

How does coarctation of the aorta present clinically?

A

Hypertension in the arms

Hypotension in the lower extremities

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42
Q

How does OSA affect blood pressure?

A

The condition produces surges in systolic and diastolic BP from sympathetic overactivity, that cause consistently raised BP at night

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43
Q

What investigation should be done if you suspect renal artery stenosis?

A

Renal USS - shows a single shrunken kidney

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44
Q

What are some signs of hypertensive retinopathy on fundoscopy?

A
  • AV nicking
  • Silver wiring
  • Cotton wool spots
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45
Q

Name 5 complications of hypertension

A
  • Stroke/TIA
  • Heart failure
  • Malignant HTN
  • MI
  • Dissecting aortic aneurysm
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46
Q

What is malignant hypertension?

A

Increased BP with acute impairment of one or more organ systems (usually BP>180/120), leading to a hypertensive emergency.

May be precipitated by the sudden discontinuation of antihypertensives.

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47
Q

What are the signs and symptoms of malignant hypertension?

A

Signs - papilloedema, retinal haemorrhage

Symptoms - nausea, haematuria, proteinuria, arrhythmias, headache, chest pain

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48
Q

How does HTN lead to HF?

A

Left ventricular hypertrophy as the heart has to pump harder to push the blood around the body

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49
Q

How does HTN lead to dissecting aortic aneurysm?

A

Hypertension causes a tear in the intimal lining of the aorta, allowing blood to enter the media and the tear to expand

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50
Q

What investigations should be done for dissecting aortic aneurysm?

A

D-dimer, CT, transesophageal ECHO, CXR

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51
Q

What are the indications and limitations of CT for cerebrovascular disease?

A

Indications - Do if suspected stroke, preferably within an hour, for patients with symptoms lasting over an hour. Can reliably exclude ICH.

Limitations - Will often be normal before 12 hours, beyond 2-3 weeks they show no difference between haemorrhage and ischaemia

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52
Q

What are the indications and limitations of MRI for cerebrovascular disease?

A

Indications - ongoing symptoms for over 14 days, particularly cerebellar/brainstem signs or disease in posterior fossa

Limitations - high cost, takes a while

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53
Q

What are the indications and limitations of angiography for cerebrovascular disease?

A

Indications - assessment for hyper acute treatment (thrombolysis/clot retrieval)

Limitations - low sensitivity

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54
Q

What are the early signs on infarction on CT?

A
  • Loss of grey/white matter differentiation
  • Loss of insular ribbon on insular cortex
  • Loss of definition of lentiform nucleus
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55
Q

What is the benefit of MRI DWI (diffusion weighted imaging)

A

Allows you to see the development of ischaemia in real time - acute lesion is bright white

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56
Q

What is the definition of an MI?

A

Tn > 99th percentile plus at least one of:

  1. Ischaemic symptoms
  2. Ischaemic ECG changes
  3. ECG evidence of necrosis (q waves)
  4. Imaging - loss of myocardium

ie. elevated troponin alone is not diagnostic

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57
Q

What are the 5 types of MI?

A

1 - usual MI, primary coronary event such as plaque rupture
2 - problem of oxygen supply and demand ie. patient doesn’t necessarily have CAD
3 - sudden cardiac death which includes signs of MI
4 - PCI associated MI (tn>x5 normal limit)
5 - CABG associated MI (tn>x10 normal), and new q waves or angiographic evidence

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58
Q

What events could cause a type 2 MI?

A

Coronary embolism
Arrhythmia
Anaemia
Hypotension

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59
Q

What does a Q wave represent?

A

Infarction of nearly the whole thickness of the myocardium

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60
Q

What is the pathophysiology of ACS?

A

Atherosclerosis leads to plaque rupture which gives off a thrombus. This can be:

  1. Occlusive - Acute MI, q wave
  2. Non-occlusive - unstable angina, NSTEMI
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61
Q

Describe a typical and atypical presentation of an MI?

A

Typical - central, crushing chest pain that radiates to the arms or jaw, accompanied by nausea, sweating, dizziness

Atypical - breathless, tachycardia, N&V, sweating (occur in elderly/diabetics)

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62
Q

Describe a typical and atypical presentation of angina?

A

Typical - (1) constricting discomfort in the chest, (2) precipitated by physical exertion and (3) relieved by rest or GTN spray in about 5 mins

Atypical - 2/3 of the above features

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63
Q

Why do we split ACS into STEMI and NSTEMI?

A

We split NSTEMI and STEMI because treatment is so different.
o STEMI – straight to cath lab and get coronary arteries opened up (urgent PCI)
o NSTEMI – there is no evidence that acute management will make a significant difference to the long-term prognosis (try to carry out PCI within 48 hours)

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64
Q

What is the ECG change that caries the highest 6 month mortality?
o T-wave inversion
o ST elevation
o ST depression

A

ACS mortality at 6 months (%)
o T-wave inversion – 3.4%
o ST elevation – 6.8%
o ST depression – 8.9%

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65
Q

What are the 3 factors that contribute to the diagnosis of ACS? (need 2 to diagnose ACS)

A
  • Chest Pain (clinical manifestation)
  • ECG changes consistent with ischaemia or necrosis. (perform immediately)
  • Elevation of cardiac markers
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66
Q

When should you take the ECG of a patient with suspected ACS?

A
  • Perform immediately
    • If ECG is normal or non diagnostic in a patient with continuing symptoms repeat after 30mins
    • If symptoms resolve repeat ECG after 2 hours – changes can occur late
    • Repeat ECG if pain persists
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67
Q

What is the implication of gross ST elevation or tombstoning on ECG

A

Go straight to PCI

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68
Q

Which leads correlate to the Anterior/Septal region of the heart? Which artery is likely to be occluded?

A

V1-V4

LAD

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69
Q

Which leads correlate to the lateral region of the heart? Which artery is likely to be occluded?

A

V5, V6, I, aVL

LCx or diagonal of LAD

70
Q

Which leads correlate to the inferior region of the heart? Which artery is likely to be occluded?

A

II, III, aVF

RCA (and/or LCx)

71
Q

Which leads correlate to the posterior region of the heart? Which artery is likely to be occluded?

A

V7-9

RCA

72
Q

What does ST depression suggest?

A

Ischaemia

73
Q

What does T wave inversion suggest?

A

Past MI/ischaemic event

74
Q

When should troponin be used as a cardiac marker?

A

Rises after 3-6 hrs, peaks at 18hr and elevated for 10 days

75
Q

What troponin measurements are required for diagnosis of acute MI?

A

Measure troponin on admission and 6-9 hours later, a troponin result >99th centile (TnT > 14) and a rise or fall of >20% on the second sample required for diagnosis of AMI.

(NB fall of 20% rules acute MI out)

76
Q

What can cause troponin elevation?

A 
Heart failure
Severe infections
Kidney disease
PE
AF
77
Q

Which troponin is used for MI diagnosis?

A

Troponin T

78
Q

Name 3 cardiac markers

A

Troponin
Myoglobin
Creatinine Kinase

79
Q

Which CK is best for cardiac damage?

A

CKmB - ratio if CKmB:Ckmm of over 5:1 indicates cardiac damage

(Ckmm = skeletal muscles)

80
Q

What is TIMI used for? What does it take into account?

A

Estimates mortality for patients with unstable angina and NSTEMI

Looks at age, RF, ASA use, presentation

81
Q

What is GRACE used for? What does it take into account?

A

Estimates admission and 6 month mortality for patients with ACS

Looks at age, HR, BP, creatinine, ST changes, troponin, Killip class and cardiac arrest

82
Q

What categories of medications are used in the treatment of ACS?

A

o Anti-ischaemic agents
o Anti-platelet agents
o Anti-thrombin agents (Fibrinolytics)
o Coronary revascularisation

83
Q

What are the drug therapies in NSTE-ACS?

A 
o	Aspirin
o	Clopidogrel / Ticagrelor
o	Fondaparinux
o	GPIIb/IIIa receptor antagonists (high risk pts only)
o	Beta blockers
o	Nitrates (if ongoing pain/LVD)
o	Statins (very good acutely and long term.)
o	ACE inhibitors
84
Q

How is STEMI managed?

A

MONAC

  • Morphine
  • Oxygen
  • Nitrates
  • Aspirin (300mg STAT)
  • Clopidogrel (300mg)

Also do PCI or thrombolysis if no contraindication
Consider heparin

85
Q

What is the post hospital discharge care for ACS?

A 
o	A	Antiplatelets and ACE-I
o	B	Beta blockers and Blood Pressure
o	C	Cholesterol and Cigarettes
o	D	Diet and Diabetes
o	E	Education and Exercise

Must review at 5wks and 3 months

86
Q

What is the definition of dyslipidemia?

A

Elevation of plasma cholesterol, triglycerides or both, or low HDL.

87
Q

What are the 5 types of lipoprotein? What do they each carry?

(order from large to small)

A
  1. Chylomicrons - carry dietary lipid
  2. VLDL - carry endogenous triglyceride
  3. Remnant VLDL or IDL - carry cholesterol and TG
  4. LDL - carry cholesterol
  5. HDL - carry cholesterol
88
Q

What is an apoprotein? What do they bind to?

A

Proteins that bind lipid to form lipoproteins

  • Apoa1 - bind HDL, GOOD
  • Apo b100 - bind remnant vldl
  • Apo b48 - bind chylomicrons
  • Lipoprotein a - binds LDL

Apo B is the worst kind as it binds atherogenic lipoproteins and is elevated in CVD

89
Q

Describe the exogenous pathway of lipid metabolism

A
  1. Dietary cholesterol and fatty acids are absorbed.
  2. Triglycerides are formed in the intestinal cell from free fatty acids and glycerol and cholesterol is esterified.
  3. Triglycerides and cholesterol combine to form chylomicrons.
  4. Chylomicrons enter the circulation and travel to peripheral sites.
  5. In peripheral tissues, free fatty acids are released from the chylomicrons to be used as energy, converted to triglyceride or stored in adipose.
  6. Remnants are used in the formation of HDL.
90
Q

Describe the endogenous pathway of lipid metabolism

A
  1. VLDL is formed in the liver from triglycerides and cholesterol esters.
  2. These can be hydrolyzed by lipoprotein lipase to form IDL or VLDL remnants.
  3. VLDL remnants are cleared from the circulation or incorporated into LDL.
  4. LDL particles contain a core of cholesterol esters and a smaller amount of triglyceride.
  5. LDL is internalized by hepatic and nonhepatic tissues.
  6. In the liver, LDL is converted into bile acids and secreted into the intestines.
  7. In non hepatic tissues, LDL is used in hormone production, cell membrane synthesis, or stored.
    LDL is also taken up by macrophages and other cells which can lead to excess accumulation and the formation of foam cells which are important in plaque formation.
91
Q

What does HDL do?

A

Reverse cholesterol transport - takes cholesterol from the tissue to the liver

92
Q

At what age does cholesterol often increase sharply?

A

Early 50s due to onset of menopause

93
Q

When should lab investigations into dyslipidemia be carried out?

A

After resolution of acute illness as this could cause increased triglycerides and decreased cholesterol

94
Q

What investigations should be done for dyslipidemia?

A 
Total cholesterol (LDL, IDL, VLDL, HDL)
Triglycerides

U&E (CKD), plasma glucose (DM) , TFTs (hypothyroidism)
LFTs (before starting statins)

95
Q

How do you calculate total atherogenic proteins (ie. non HDL-C)

A

TC - HDL-C

Use when patient isn’t fasting and to assess response to treatment

96
Q

How do you calculate LDL-C? When is this calculation used?

A

TC - (HDL-C + TG/2.2)

This is known as the Friedewald equation.
The patient must have 12h fasting TG<4.5 before calculating this.
Used to diagnose familial hypercholesterolaemia

97
Q

What is the mechanism of familial hypercholesterolaemia?

A

Reduction (heterozygous) or absence (homozygous) of receptor mediated clearance of LDL, due to mutation of LDLR, ApoB or PCSK9 gene

98
Q

What is the lipid profile of familial hypercholesterolaemia?

A
  • Elevated LDL-C
  • Elevated cholesterol
  • Low/normal TGs
99
Q

How is familial hypercholesterolaemia inherited?

A

Autosomal dominant

100
Q

What are the physical signs of familial hypercholesterolaemia?

A

Heterozygous:

  • Tendon xanthomas
  • Corneal arcus
  • Xanthelasmas

Homozygous:

  • Cutaneous xanthomas (digital/nasal cleft)
  • Aortic stenosis
101
Q

Which dyslipidemias have the highest risk of cardiovascular complications?

A

FAMILIAL HYPERCHOLESTEROLAEMIA - VERY HIGH RISK OF SUDDEN CARDIAC DEATH

Homoxygous patients need early genetic testing and plasmaphoresis to take out LDLs

(remnant type also has high risk_

102
Q

What are the 3 types of hypertriglyceridaemia?

A
  • Polygenic
  • Familial
  • Lipoprotein lipase deficiency and apoprotein C11 deficiency
103
Q

How does hypertriglyceridaemia present?

A
  • Eruptive xanthomas
  • Lipaemia retinalis (thrombosis)
  • Acute pancreatitis
  • Metabolic syndrome
  • DM
104
Q

What is the mechanism behind hypertriglyceridaemia?

A

Disorderd triglyceride metabolism

105
Q

What is the lipid profile of familial hypertriglyceridaemia?

A
  • Elevated TG
  • Normal ApoB
  • Low HDL-C
106
Q

What is the mechanism behind familial combined hyperlipidemia?

A

Overproduction of VLDL and apoB, multigenic cause

107
Q

What is the lipid profile of familial combined hyperlipidemia?

A
  • Elevated total cholesterol
  • Elevated LDL-C
  • Elevated TG
  • Low HDL-C
108
Q

What are the physical signs of familial combined hyperlipidemia?

A
  • Non-specific

- Xanthelasma

109
Q

What is the most common inherited dyslipidemia?

A

COMBINED

110
Q

What is the mechanism of remnant (type 3) hyperlipidemia?

A

Reduction in receptor mediated clearance of remnants, due to homozygosity for the ApoE2 waveform (autosomal recessive)

These remnants are incorporated into macrophages in the process of atherosclerosis

111
Q

What is the lipid profile of remnant hyperlipidemia?

A

CHARACTERISTIC LOW APOB

  • Elevated total cholesterol
  • ELevated TG
  • Presence of VLDL remnants
112
Q

What are the physical signs of remnant hyperlipidemia?

A
  • Striate palmar xanthomas on palms

- Tuberoeruptive xanthomas on elbows and knees

113
Q

How is CVD risk looked at for a patient with dyslipidemia ?

A

QRISK - if 10yr score is over 10%, start on statins

114
Q

How is high TG treated?

A

Fibrates, omega-3 fatty acids

115
Q

How is high cholesterol treated?

A

Statins
or
Exetimibe + fibrates

116
Q

How is combined treated?

A

Statins, fibrates, nicotinic acid

117
Q

What are the side effects of statins?

A

Liver enzyme elevation

Rhabdomyolysis (high CK)

118
Q

How do statins work?

A

HMG CoA reductase inhibitor

119
Q

If a patient has had a stroke should they be started on a statin?

A

YES - regardless of their cholesterol level.

120
Q

What are the uses and limitations of LDL-C and non HDL-C?

A
  • LDL-C is important for diagnosis of Familial Hypercholesterolaemia
  • Non-HDL-C is preferred for assessment of response to treatment
  • Both LDL-C and Non-HDL-C can be used as treatment targets.
    • BUT Calculation of LDL-C assumes a constant Cholesterol /TG ratio in VLDL, which requires fasting to ensure absence of postprandial lipoproteins, including chylomicrons and chylomicron remnants

• Fasting only matters if you are trying to accurately measure LDL. Non HDL-C doesn’t require fasting

121
Q

What can apolipoproteins be used for?

A

Apolipoprotein can be used to assess risk and as treatment targets

122
Q

When can QRISK2 not be used?

A

Q risk 2 is not used in people who are already high risk, e.g.:
o Due to familial/inherited dyslipidaemias
o People with pre-existing CVD
o CKD with eGFR < 60
o Type I DM
o People aged 85 or older who are at increased risk of CVD because of age alone, particularly those who smoke or have raised blood pressure

123
Q

What is the definition of cardiac syncope?

A

Temporary LOC due to insufficient blood flow to the brain - this may not be prodromal and will have a rapid recovery.

124
Q

What are the red flags for syncope?

A
  • Rapid recovery

- Pre-existing cardiac history or fam hx

125
Q

What is the commonest cause of SCD in the UK?

A

Coronary artery disease

126
Q

What else may cause cardiac syncope or SCD?

A
  • Arrhythmias (WPW, VT, nodal block)
  • Valvular heart disease
  • PE
  • Cardiomyopathies (HCOM, dilated, ARVC)
  • Aortic dissection
  • Channelopathies (brugada, long QT syndrome)
127
Q

What is the definition of sudden death?

A

A death of natural causes, occurring within 1hr of symptom onet

128
Q

What investigations should be done for a pt with cardiac disease?

A
  • ECG
  • Echo
  • Heart monitors (hotter ECG, zio patch, memo, implantable loop recorder)
  • Genetic testing
129
Q

What is the pathophysiology of WPW syndrome?

A

Abnormal accessory pathway between the atria and the ventricles, which conducts electrical activity at a higher rate than the AV node - this means AF goes straight to VF

130
Q

What does ECG show in WPW syndrome?

A 
Delta waves (slurred up in QRS complex)
Short PR interval
131
Q

How is WPW treated?

A

Ablation of accessory pathway

132
Q

What is the pathophysiology of HCOM?

A

Autosomal dominant mutation in sarcomere gene, leading to increased size of myocytes, leading to abnormal alignment of muscle cells and ‘tangles’ - these cause turbulence in the heart with regional differences

133
Q

What is the leading cause of SCD in young athletes?

A

HCOM

134
Q

How should HCOM be investigated?

A

ECHO (diagnostic)

ECG, cardiac MRI, catheterization

135
Q

How is HCOM treated?

A

Asymptomatic - none, screening

Symptomatic (presents like HF) - beta blockers, surgical septal myectomy, septal ablation, ICD, mitral clip

136
Q

What is the only definitive treatment for HCOM?

A

ICD

137
Q

What is the pathophysiology of ARVC?

A

Arrhythmogenic right ventricular cardiomyopathy
Inherited condition in which clusters of fat and fibrous tissue get deposited between cells, due to weakened connection proteins between the myocytes.

Ventricles get thin and stretched, patients more prone to arrhythmias

138
Q

How is ARVC diagnosed?

A

ECG shows epsilon waves, RBBB and T wave inversion

139
Q

What does an epsilon wave look like?

A

Small positive deflection at end of QRS complex

140
Q

What is the pathophysiology of dilated cardiomyopathy? What causes it?

A

Dilation and scarring of left ventricle due to

  • previous MI
  • viral
  • toxic agents
  • autoimmune
  • alcohol
  • genetics

As DCM progreses, further damage accumulates leading to chronic heart failure

141
Q

How is DCOM investigated?

A

MRI - white stripes of scar tissue

ECG changes

142
Q

What is the most common arrhythmia in cardiomyopathy?

A

A mix of monomorphic VT and VF

143
Q

What is the pathophysiology of brugada syndrome?

A

Mutation in a gene that encodes for the sodium channel in the myocytes
Results in regional differences of conduction across the myocardium

‘Young man that dies in the night’

144
Q

What ECG changes are seen with brugada syndrome?

A

Type 1 - coved
Type 2- saddle back

ST elevation from V1-3
RBBB brought on by ajalmine admin

145
Q

What is the most common arrhythmia in channelopathies?

A

Polymorphic VT and VF

146
Q

What are the criteria for brugada syndrome?

A 
o	VF/polymorphic VT
o	Fam hx of SCD <45 yrs
o	Similar ECGs in family members
o	Syncope
o	VT able to be induced electrically (‘ecg inside the heart’)
o	Nocturnal agonal respiration
147
Q

How is brugada syndrome treated?

A

Fleconide (Na channel blocker) to prevent AF

148
Q

What is the pathophysiology of long QT syndrome?

A

Delayed repolarisation of the heart following a heartbeat, which increases the risk of episodes of TORSADES DE POINTES

149
Q

What are the characteristic clinical features of long QT syndrome?

A

Black out with exercise, swimming or ‘startle reflex’

150
Q

What channel is commonly involved in LQTS?

A

Potassium

151
Q

How is LQTS treated?

A

Beta blockers
K supplements
Mexiletine

152
Q

What does q wave on ECG indicate?

A

Current or prior MI

153
Q

What does bifascicular block on ECG indicate?

A

Bifasicular block = RBBB and left axis deviation (sign of wear and tear).

154
Q

What does a trifascicular block on ECG indicate?

A

Trifasicular block = 1st degree heart block (prolonged PR), RBBB & left axis deviation

155
Q

What is catecholaminergic polymorphic VT?

A

Exercise/emotion induced life threatening tachycardias, due to mutations in the calcium channel

156
Q

What is the diagnostic investigation in CPVT?

A

Exercise test - shows irregularly shaped ventricular arrhytmias

(would give normal ECG)

157
Q

What would first degree heart block look like on ECG?

A

Long PR interval

158
Q

What would second degree heart block look like on ECG?

A

Mobitz type 1 (Wenkenbacks) - longer and longer PR interval until there is a p wave with no QRS complex

Mobitz type 2 - some p waves not followed by QRS complexes

159
Q

What would third degree (complete) heart block look like on ECG?

A

No relationship at all between p waves and QRS complexes - can lead to sudden cardiac death

160
Q

How is paroxysmal AF managed?

A

Beta blockers

Oral flecainide PRN in times of attack

161
Q

What is the risk of mitral valve prolapse?

A

Endocarditis

162
Q

What is the management of malignant hypertension?

A

Sodium nitroprusside - need to do intra-arterial BP monitoring to check the patient is not too hypertensive

163
Q

How is HCOM treated 1st line?

A

Beta blockers

164
Q

What test is diagnostic for aortic dissection?

A

CT/MRI

165
Q

Which murmur is atrial fibrillation most associated with?

A

Mitral stenosis

166
Q

What is the best management of persistant/permanent AF?

A

Rate control and anticoag

eg. bisoprolol + verapamil + warfarin

167
Q

What are the two shockable rhythms?

A

Ventricular fibrillation

Sustained ventricular tachy (shows cannon a waves on JVP waveform)

168
Q

In what presentation are there ‘absent a waves’ on JVP waveform?

A

Atrial fibrillation

169
Q

If a patient has a CHADVAS score of 0, what is the management?

A

Aspirin

170
Q

If a patient has a CHADVAS score of 1 what is the management?

A

Aspirin or warfarin

171
Q

If a patient has a CHADVAS score of 2, what is the management?

A

Warfarin

172
Q

What would the PR interval be in WPW syndrome?

A

<120, due to accessory pathway

4TH YEAR - CSIM2 (20 decks)

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