Vascular Medicine Flashcards
(172 cards)
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
2
Q
What is the pathogenesis of atherosclerosis?
A
- LDL particles migrate to arteries and oxidise, forming a fatty layer
- This attracts monocytes which expand at the site to form foam cells
- Foam cells accumulate to form a plaque
- Smooth muscle cells move to the intimate and contribute to the formation of a fibrous cap
- Over time this narrows the lumen, leading to reduced blood flow
- The cap releases collagen and elastin causing the plaque to rupture
- When the plaque ruptures, thrombosis is triggered and clots form which further impede blood flow
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.
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
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.
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
7
Q
How is acute limb ischaemia managed?
A
Open surgery, angioplasty, thrombolysis, anticoagulation
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)
9
Q
What is the 1st line imaging for PAD?
A
Colour duplex ISS
10
Q
Name some cardiovascular risk factors
A
- Smoking
- Age
- Hyperlipidemia
- Hypertension
- DM
- Previous CVD
- Ethnicity
- Fam hx
11
Q
What are the features of the metabolic syndrome?
A
- Insulin resistance
- Central obesity
- Hypertension
- Dyslipidemia
- Impaired glucose tolerance
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)
13
Q
What is the single biggest risk factor for having a recurrent stroke having had a single TIA?
A
Hypertension
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.
15
Q
What is the definition of hypertension?
A
BP greater than or equal to 140/90mmHg
16
Q
What is the main cause of hypertension?
A
Essential HTN (80%) - complex interaction of genes and environment
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
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
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.
20
Q
How does renovascular disease affect blood pressure?
A
Stenosis to the kidneys will activate the RAAS causing an increase in BP
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.
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)
23
Q
What potent circulating vasodepressor are many patients with renal disease deficient in?
A
Medullipin - this would usually lower pp
24
Q
Describe the development of salt sensitive hypertension
A
- Exposure to stimuli that causes renal vasoconstriction
- Renal injury caused by tubular ischemia, causing impaired sodium excretion
- Sodium excretion restored to equal intake at the expense of shift to higher systemic blood pressure
25
How does Conn's syndrome affect blood pressure? What is the typical biochem?
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
26
What investigations should be done for someone with Conn's?
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.
27
How does Cushings syndrome affect blood pressure?
Excess cortisol binds to the aldosterone receptor, activating RAAD
28
What investigations should be done for someone with Cushing's?
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)
29
How does Pheochromocytoma affect blood pressure?
Adrenal catecholamine-secreting tumour - catecholamines increase HR, causing vasoconstriction and sodium retention, leading to postural hypotension and labile BP.
30
What are the symptoms of phaeochromocytoma?
Labile BP
Postural hypotension
Headache
Many asymptomatic
31
Which syndromes is phaeochromocytoma associated with?
Von Hipper Lindau syndrome
| MEN 2
32
What investigations should be done for someone with pheochromocytoma?
- Plasma free mets (diagnostic)
| - Urinary catecholamines (less convenient
33
What is shuttle enzyme deficiency?
A condition causing 'apparent aldosterone excess'
- failure of conversion from cortisol to cortisone (which would usually deactivate it)
- hypertension
34
Which enzyme is deficient in shuttle enzyme deficiency?
11B-HSD
35
What is Liddles syndrome?
Genetic disorder causing increased activity of epithelial sodium channel so it is constantly open
- kidney excretes more potassium but retains sodium and water
36
What are the clinical and biochemical features of Liddle's syndrome?
CLINICAL - autosomal dominant, early onset HTN
BIOCHEM - low K, metabolic alkalosis, high bicarb, low aldosterone, high sodium
37
How is Liddle's syndrome investigated and managed?
INVESTIGATION - Bloods, ABG, genetic testing
MANAGEMENT - amiloride
38
How does acromegaly affect blood pressure?
Chronic exposure to GH and IGF-1 causes RAAS activation.
| Also, associated insulin resistance increases BP
39
What are the components of routine assessment of raised BP?
- BP
- Height/weight/BMI
- Pulses (radio femoral delay = coarctation)
- Kidneys (palpable = PCKD)
- End organ damage (U&E, creatinine, ECG)
- Fundoscopy
40
What is the indication for ambulatory blood pressure monitoring?
Clinic BP 140/90 or higher
41
How does coarctation of the aorta present clinically?
Hypertension in the arms
| Hypotension in the lower extremities
42
How does OSA affect blood pressure?
The condition produces surges in systolic and diastolic BP from sympathetic overactivity, that cause consistently raised BP at night
43
What investigation should be done if you suspect renal artery stenosis?
Renal USS - shows a single shrunken kidney
44
What are some signs of hypertensive retinopathy on fundoscopy?
- AV nicking
- Silver wiring
- Cotton wool spots
45
Name 5 complications of hypertension
- Stroke/TIA
- Heart failure
- Malignant HTN
- MI
- Dissecting aortic aneurysm
46
What is malignant hypertension?
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.
47
What are the signs and symptoms of malignant hypertension?
Signs - papilloedema, retinal haemorrhage
| Symptoms - nausea, haematuria, proteinuria, arrhythmias, headache, chest pain
48
How does HTN lead to HF?
Left ventricular hypertrophy as the heart has to pump harder to push the blood around the body
49
How does HTN lead to dissecting aortic aneurysm?
Hypertension causes a tear in the intimal lining of the aorta, allowing blood to enter the media and the tear to expand
50
What investigations should be done for dissecting aortic aneurysm?
D-dimer, CT, transesophageal ECHO, CXR
51
What are the indications and limitations of CT for cerebrovascular disease?
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
52
What are the indications and limitations of MRI for cerebrovascular disease?
Indications - ongoing symptoms for over 14 days, particularly cerebellar/brainstem signs or disease in posterior fossa
Limitations - high cost, takes a while
53
What are the indications and limitations of angiography for cerebrovascular disease?
Indications - assessment for hyper acute treatment (thrombolysis/clot retrieval)
Limitations - low sensitivity
54
What are the early signs on infarction on CT?
- Loss of grey/white matter differentiation
- Loss of insular ribbon on insular cortex
- Loss of definition of lentiform nucleus
55
What is the benefit of MRI DWI (diffusion weighted imaging)
Allows you to see the development of ischaemia in real time - acute lesion is bright white
56
What is the definition of an MI?
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
57
What are the 5 types of MI?
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
58
What events could cause a type 2 MI?
Coronary embolism
Arrhythmia
Anaemia
Hypotension
59
What does a Q wave represent?
Infarction of nearly the whole thickness of the myocardium
60
What is the pathophysiology of ACS?
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
61
Describe a typical and atypical presentation of an MI?
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)
62
Describe a typical and atypical presentation of angina?
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
63
Why do we split ACS into STEMI and NSTEMI?
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)
64
What is the ECG change that caries the highest 6 month mortality?
o T-wave inversion
o ST elevation
o ST depression
ACS mortality at 6 months (%)
o T-wave inversion – 3.4%
o ST elevation – 6.8%
o ST depression – 8.9%
65
What are the 3 factors that contribute to the diagnosis of ACS? (need 2 to diagnose ACS)
- Chest Pain (clinical manifestation)
- ECG changes consistent with ischaemia or necrosis. (perform immediately)
- Elevation of cardiac markers
66
When should you take the ECG of a patient with suspected ACS?
- 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
67
What is the implication of gross ST elevation or tombstoning on ECG
Go straight to PCI
68
Which leads correlate to the Anterior/Septal region of the heart? Which artery is likely to be occluded?
V1-V4
| LAD
69
Which leads correlate to the lateral region of the heart? Which artery is likely to be occluded?
V5, V6, I, aVL
| LCx or diagonal of LAD
70
Which leads correlate to the inferior region of the heart? Which artery is likely to be occluded?
II, III, aVF
| RCA (and/or LCx)
71
Which leads correlate to the posterior region of the heart? Which artery is likely to be occluded?
V7-9
| RCA
72
What does ST depression suggest?
Ischaemia
73
What does T wave inversion suggest?
Past MI/ischaemic event
74
When should troponin be used as a cardiac marker?
Rises after 3-6 hrs, peaks at 18hr and elevated for 10 days
75
What troponin measurements are required for diagnosis of acute MI?
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
What can cause troponin elevation?
```
Heart failure
Severe infections
Kidney disease
PE
AF
```
77
Which troponin is used for MI diagnosis?
Troponin T
78
Name 3 cardiac markers
Troponin
Myoglobin
Creatinine Kinase
79
Which CK is best for cardiac damage?
CKmB - ratio if CKmB:Ckmm of over 5:1 indicates cardiac damage
(Ckmm = skeletal muscles)
80
What is TIMI used for? What does it take into account?
Estimates mortality for patients with unstable angina and NSTEMI
Looks at age, RF, ASA use, presentation
81
What is GRACE used for? What does it take into account?
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
What categories of medications are used in the treatment of ACS?
o Anti-ischaemic agents
o Anti-platelet agents
o Anti-thrombin agents (Fibrinolytics)
o Coronary revascularisation
83
What are the drug therapies in NSTE-ACS?
```
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
How is STEMI managed?
MONAC
- Morphine
- Oxygen
- Nitrates
- Aspirin (300mg STAT)
- Clopidogrel (300mg)
Also do PCI or thrombolysis if no contraindication
Consider heparin
85
What is the post hospital discharge care for ACS?
```
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
What is the definition of dyslipidemia?
Elevation of plasma cholesterol, triglycerides or both, or low HDL.
87
What are the 5 types of lipoprotein? What do they each carry?
(order from large to small)
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
What is an apoprotein? What do they bind to?
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
Describe the exogenous pathway of lipid metabolism
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
Describe the endogenous pathway of lipid metabolism
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
What does HDL do?
Reverse cholesterol transport - takes cholesterol from the tissue to the liver
92
At what age does cholesterol often increase sharply?
Early 50s due to onset of menopause
93
When should lab investigations into dyslipidemia be carried out?
After resolution of acute illness as this could cause increased triglycerides and decreased cholesterol
94
What investigations should be done for dyslipidemia?
```
Total cholesterol (LDL, IDL, VLDL, HDL)
Triglycerides
```
U&E (CKD), plasma glucose (DM) , TFTs (hypothyroidism)
LFTs (before starting statins)
95
How do you calculate total atherogenic proteins (ie. non HDL-C)
TC - HDL-C
Use when patient isn't fasting and to assess response to treatment
96
How do you calculate LDL-C? When is this calculation used?
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
What is the mechanism of familial hypercholesterolaemia?
Reduction (heterozygous) or absence (homozygous) of receptor mediated clearance of LDL, due to mutation of LDLR, ApoB or PCSK9 gene
98
What is the lipid profile of familial hypercholesterolaemia?
- Elevated LDL-C
- Elevated cholesterol
- Low/normal TGs
99
How is familial hypercholesterolaemia inherited?
Autosomal dominant
100
What are the physical signs of familial hypercholesterolaemia?
Heterozygous:
- Tendon xanthomas
- Corneal arcus
- Xanthelasmas
Homozygous:
- Cutaneous xanthomas (digital/nasal cleft)
- Aortic stenosis
101
Which dyslipidemias have the highest risk of cardiovascular complications?
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
What are the 3 types of hypertriglyceridaemia?
- Polygenic
- Familial
- Lipoprotein lipase deficiency and apoprotein C11 deficiency
103
How does hypertriglyceridaemia present?
- Eruptive xanthomas
- Lipaemia retinalis (thrombosis)
- Acute pancreatitis
- Metabolic syndrome
- DM
104
What is the mechanism behind hypertriglyceridaemia?
Disorderd triglyceride metabolism
105
What is the lipid profile of familial hypertriglyceridaemia?
- Elevated TG
- Normal ApoB
- Low HDL-C
106
What is the mechanism behind familial combined hyperlipidemia?
Overproduction of VLDL and apoB, multigenic cause
107
What is the lipid profile of familial combined hyperlipidemia?
- Elevated total cholesterol
- Elevated LDL-C
- Elevated TG
- Low HDL-C
108
What are the physical signs of familial combined hyperlipidemia?
- Non-specific
| - Xanthelasma
109
What is the most common inherited dyslipidemia?
COMBINED
110
What is the mechanism of remnant (type 3) hyperlipidemia?
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
What is the lipid profile of remnant hyperlipidemia?
CHARACTERISTIC LOW APOB
- Elevated total cholesterol
- ELevated TG
- Presence of VLDL remnants
112
What are the physical signs of remnant hyperlipidemia?
- Striate palmar xanthomas on palms
| - Tuberoeruptive xanthomas on elbows and knees
113
How is CVD risk looked at for a patient with dyslipidemia ?
QRISK - if 10yr score is over 10%, start on statins
114
How is high TG treated?
Fibrates, omega-3 fatty acids
115
How is high cholesterol treated?
Statins
or
Exetimibe + fibrates
116
How is combined treated?
Statins, fibrates, nicotinic acid
117
What are the side effects of statins?
Liver enzyme elevation
| Rhabdomyolysis (high CK)
118
How do statins work?
HMG CoA reductase inhibitor
119
If a patient has had a stroke should they be started on a statin?
YES - regardless of their cholesterol level.
120
What are the uses and limitations of LDL-C and non HDL-C?
- 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
What can apolipoproteins be used for?
Apolipoprotein can be used to assess risk and as treatment targets
122
When can QRISK2 not be used?
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
What is the definition of cardiac syncope?
Temporary LOC due to insufficient blood flow to the brain - this may not be prodromal and will have a rapid recovery.
124
What are the red flags for syncope?
- Rapid recovery
| - Pre-existing cardiac history or fam hx
125
What is the commonest cause of SCD in the UK?
Coronary artery disease
126
What else may cause cardiac syncope or SCD?
- Arrhythmias (WPW, VT, nodal block)
- Valvular heart disease
- PE
- Cardiomyopathies (HCOM, dilated, ARVC)
- Aortic dissection
- Channelopathies (brugada, long QT syndrome)
127
What is the definition of sudden death?
A death of natural causes, occurring within 1hr of symptom onet
128
What investigations should be done for a pt with cardiac disease?
- ECG
- Echo
- Heart monitors (hotter ECG, zio patch, memo, implantable loop recorder)
- Genetic testing
129
What is the pathophysiology of WPW syndrome?
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
What does ECG show in WPW syndrome?
```
Delta waves (slurred up in QRS complex)
Short PR interval
```
131
How is WPW treated?
Ablation of accessory pathway
132
What is the pathophysiology of HCOM?
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
What is the leading cause of SCD in young athletes?
HCOM
134
How should HCOM be investigated?
ECHO (diagnostic)
ECG, cardiac MRI, catheterization
135
How is HCOM treated?
Asymptomatic - none, screening
| Symptomatic (presents like HF) - beta blockers, surgical septal myectomy, septal ablation, ICD, mitral clip
136
What is the only definitive treatment for HCOM?
ICD
137
What is the pathophysiology of ARVC?
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
How is ARVC diagnosed?
ECG shows epsilon waves, RBBB and T wave inversion
139
What does an epsilon wave look like?
Small positive deflection at end of QRS complex
140
What is the pathophysiology of dilated cardiomyopathy? What causes it?
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
How is DCOM investigated?
MRI - white stripes of scar tissue
| ECG changes
142
What is the most common arrhythmia in cardiomyopathy?
A mix of monomorphic VT and VF
143
What is the pathophysiology of brugada syndrome?
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
What ECG changes are seen with brugada syndrome?
Type 1 - coved
Type 2- saddle back
ST elevation from V1-3
RBBB brought on by ajalmine admin
145
What is the most common arrhythmia in channelopathies?
Polymorphic VT and VF
146
What are the criteria for brugada syndrome?
```
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
How is brugada syndrome treated?
Fleconide (Na channel blocker) to prevent AF
148
What is the pathophysiology of long QT syndrome?
Delayed repolarisation of the heart following a heartbeat, which increases the risk of episodes of TORSADES DE POINTES
149
What are the characteristic clinical features of long QT syndrome?
Black out with exercise, swimming or 'startle reflex'
150
What channel is commonly involved in LQTS?
Potassium
151
How is LQTS treated?
Beta blockers
K supplements
Mexiletine
152
What does q wave on ECG indicate?
Current or prior MI
153
What does bifascicular block on ECG indicate?
Bifasicular block = RBBB and left axis deviation (sign of wear and tear).
154
What does a trifascicular block on ECG indicate?
Trifasicular block = 1st degree heart block (prolonged PR), RBBB & left axis deviation
155
What is catecholaminergic polymorphic VT?
Exercise/emotion induced life threatening tachycardias, due to mutations in the calcium channel
156
What is the diagnostic investigation in CPVT?
Exercise test - shows irregularly shaped ventricular arrhytmias
(would give normal ECG)
157
What would first degree heart block look like on ECG?
Long PR interval
158
What would second degree heart block look like on ECG?
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
What would third degree (complete) heart block look like on ECG?
No relationship at all between p waves and QRS complexes - can lead to sudden cardiac death
160
How is paroxysmal AF managed?
Beta blockers
| Oral flecainide PRN in times of attack
161
What is the risk of mitral valve prolapse?
Endocarditis
162
What is the management of malignant hypertension?
Sodium nitroprusside - need to do intra-arterial BP monitoring to check the patient is not too hypertensive
163
How is HCOM treated 1st line?
Beta blockers
164
What test is diagnostic for aortic dissection?
CT/MRI
165
Which murmur is atrial fibrillation most associated with?
Mitral stenosis
166
What is the best management of persistant/permanent AF?
Rate control and anticoag
| eg. bisoprolol + verapamil + warfarin
167
What are the two shockable rhythms?
Ventricular fibrillation
| Sustained ventricular tachy (shows cannon a waves on JVP waveform)
168
In what presentation are there 'absent a waves' on JVP waveform?
Atrial fibrillation
169
If a patient has a CHADVAS score of 0, what is the management?
Aspirin
170
If a patient has a CHADVAS score of 1 what is the management?
Aspirin or warfarin
171
If a patient has a CHADVAS score of 2, what is the management?
Warfarin
172
What would the PR interval be in WPW syndrome?
<120, due to accessory pathway
