Cardio Flashcards

1
Q

What are the key risk factors for IHD?

A
  • Smoking
  • HTN
  • DM
  • Hypercholesterolaemia
  • FHx (+ve = first degree relative with symptomatic CAD in their 50s if male or 60s if female)
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2
Q

PC : Chest pain

What do you look for on examination?

A
  • Signs of acute HF - raised JVP, pulmonary oedema, leg swelling
  • Signs of cariogenic shock - mottling, thready pulses
  • Valve lesion - critical AS, acute MR, acute AR
  • Features of aortic dissection - pulse differences, neurological defects
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3
Q

PC: Chest pain

What investigations do you do?

A
  • Obs
  • Bloods - FBC, U+E, clotting, troponin +/- d-dimer
  • ECG
  • CXR -PE/pneumothorax
  • ABG - if hypoxic/PE suspected
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4
Q

What are potential end results of atherosclerosis?

A
  • Angina
  • MI
  • TIA
  • Stroke
  • PAD
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5
Q

What is used to guide primary prevention of cardiovascular disease? What is given?

A
  • QRSIK3
  • When the result is >10% they should be offered a statin
  • Initially atorvastatin 20mg at night
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6
Q

What should be checked after starting a statin?

A
  • Lipids 3 months after starting, increase the dose to achieve a >40% reduction in non-HDL cholesterol
  • LFTs within 3 months of starting a statin and again at 12 months. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use
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7
Q

What are potential side effects of statins?

A
  • Myopathy (muscle weakness and pain)
  • Rhabdomyolysis (muscle damage - check the creatine kinase in pts with muscle pain)
  • Type 2 diabetes
  • Haemorrhagic strokes (rare)
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8
Q

What medications interact with statins?

A

Macrolide abx e.g. clarithromycin

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9
Q

What is familial hypercholesterolaemia?

A

An autosomal dominant genetic condition causing very high cholesterol levels

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10
Q

What criteria are used for making a diagnosis of familial hypercholesterolaemia? What do they include?

A

The Simon Broome criteria or the Dutch Lipid Clinic Network Criteria
- FHx of premature cardiovascular disease (e.g. myocardial infarction under 60 in a first-degree relative)
- Very high cholesterol (>7.5 mmol/L)
- Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)

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11
Q

What is angina caused by?

A

Atherosclerosis

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12
Q

When is angina ‘stable’?

A

When it is caused by exercise and relieved by rest or GTN

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13
Q

Other than bloods what investigations are used in angina?

A
  • Cardiac stress testing
  • CT coronary angiography
  • Invasive coronary angiography
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14
Q

What are the principles of angina management?

A

RAMPS

R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention

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15
Q

What is used for immediate symptomatic relief of angina? How is it taken?

A
  • Sublingual GTN
  • Take the GTN when the symptoms start
  • Take a second dose after 5 minutes if the symptoms remain
  • Take a third dose after a further 5 minutes if the symptoms remain
  • Call an ambulance after a further 5 minutes if the symptoms remain
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16
Q

What is used for long-term symptomatic relief of angina?

A
  • BB
  • CCB
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17
Q

What is the management of stable angina?

A

4 A’s

A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if DM, HTN, CKD, HF are present)
A – Antianginals - BB, CCB, nitrates

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18
Q

When are pts wit stable angina referred for intervention? What are the options?

A
  • If failed on 2 antianginals
  • Percutaneous coronary intervention (PCI)
  • Coronary artery bypass graft (CABG)
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19
Q

What are 2 key side effects of GTN? What causes them?

A
  • Headaches
  • Dizzness
  • Vasodilation
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20
Q

What are 3 types of acute coronary syndrome (ACS)?

A
  • Unstable angina
  • ST-elevation myocardial infarction
  • NSTEMI
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21
Q

What usually causes ACS?

A

A thrombus from an atherosclerotic plaque blocking a coronary artery

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22
Q

What ECG changes do you get in STEMI?

A
  • ST-segment elevation
  • New left bundle branch block
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23
Q

What ECG changes do you get in NSTEMI?

A
  • ST segment depression
  • T wave inversion
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24
Q

What does troponin indicate? What is it used to diagnosed?

A
  • Myocardial ischaemic
  • STEMI/NSTEMI
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25
When should you measure troponin? How do you interpret it?
Troponin goes up after 5/6 hrs and peaks at 2 days - Measure ASAP - If raised measure again in 3hrs - sig rise/fall = MI - If not raised can rule out MI unless pain was <6hrs ago (in this case measure again at 6 hrs)
26
When is a diagnosis of unstable angina given?
- Symptoms of ACS - Normal ECG - Normal troponin
27
What is the acute management of MI?
MONA: - Morphine - only if needed, give with metaclopramide - Oxygen - only to maintain sats - Nitrates - 2 puffs sublingual - Aspirin - 300mg stat If meets criteria and within 2 hrs of presentation -> refer for PCI. If not, consider thrombolysis
28
What are the criteria for PCI in STEMI?
- ST elevation >2mm in 2 contiguous chest leads or >1mm in 2 contiguous limb leads - Chest pain - New LBBB is often considered an indication for PCI in the right clinical context
29
Was is the FY1 management of NSTEMI?
- Cardiac monitoring - Management of complications - Load with P2Y12 inhibitor - ticagrelor 180mg - Clopidogrel (2nd line) - Anticoagulation (fondaparinux) - Seek senior help
30
When is PCI considered in NSTEMI?
- Unstable patients - According to their GRACE score (medium/high risk = considered)
31
What is the GRACE score?
- Gives a 6-month probability of death after having an NSTEMI - Above 3% is considered medium to high risk
32
What meds should be on someones TTO following an MI?
The big 5: - Aspirin 75mg OD indefinitely - Potent P2Y12 inhibitor - ticagrelor 90mg BD for >1 year (antiplatelet) - Cardioselective BB - bisoprolol 2.5mg OD - ACE-In - ramipril 2.5mg - High intensity statin - atorvastatin 80mg OD (PRN GTN)
33
What is the FU for an MI?
- Clinic in 1 month - TTE if not had as IP - Cardiac rehabilitation programme - Smoking cessation - GP - uptitrate secondary prevention
34
What advice do you give to pts following an MI?
- Don't drive for 1 week if PCI, 4 weeks if no PCI - Gradually return to usual activity levels - 6 weeks off work - Stop smoking
35
Dressler's syndrome: 1. What is it? 2. How does it present? 3. Investigations 4. Management
1. Post-myocardial infarction syndrome. Caused by localised immune response that results in inflammation of the pericardium 2. Pleuritic chest pain, fever, pericardial rub on auscultation 3. ECG (widespread ST elevation and T wave inversion) , echo (pericardial effusion), inflammatory markers (raised) 4. NSAIDS, steroids in more severe cases
36
What happens in acute left ventricular heart failure?
- An acute event results in the LV being unable to move blood efficiently through the left side of the heart - This results in raised pulmonary pressure and pulmonary oedema - This interferes with normal gas exchange in the lungs, causing SOB and reduced O2 saturation
37
What are potential triggers of acute LV heart failure?
- Iatrogenic (e.g. aggressive IV fluids in a frail elderly patient with impaired LV function) - MI - Arrhythmias - Sepsis - Hypertensive emergency (acute, severe increase in BP)
38
A nurse asks you to review a a breathless and desaturating patient. They are 85 years old with chronic kidney disease and aortic stenosis. What should you check? How would you manage the likely issues?
Acute left ventricular failure and pulmonary oedema are common in the acute hospital setting - How much fluid that patient has been given and whether they will be able to cope with that amount - IV furosemide to clear the excess fluid - world well in improving symptoms
39
What signs would indicate acute LV heart failure on examination?
- Raised respiratory rate - Reduced oxygen saturations - Tachycardia - 3rd heart sound - Bilateral basal crackles (sounding “wet”) on auscultation of the lungs If they also have R sided HF - raised JVP, peripheral oedema
40
What can CXR show in acute LV heart failure?
- Cardiomegaly - Upper lobe diversion (upper lobe veins are enlarged due to back pressure) - Bilateral pleural effusions - Fluid in interlobar fissures (between the lung lobes) - Kerley lines (fluid in the septal lines)
41
What is the initial management of a patient with acute LV heart failure?
S – Sit up O – Oxygen D – Diuretics I – Intravenous fluids should be stopped U – Underlying causes need to be identified and treated (e.g., myocardial infarction) M – Monitor fluid balance
42
What are the first line and diagnostic investigations for heart failure?
- NT-proBNP - Echocardiogram
43
Other than HF, what issues can cause raised BnP?
Sepsis, renal problems, COPD
44
What are poor prognostic factors in HF?
- Smoking - Increasing age - Low BMI - Obesity - Diabetes
45
Explain how the causes of chronic HF be classified
- High output - the heart is working at a normal rate but is unable to meet the demands of the body - Low output - decreased heart function
46
Causes of high output chronic HF
- Hyperthyroidism - Anaemia - Paget's disease - AV malformation
47
How can low output chronic HF be further classified?
- Increased pre-load - Pump failure - Chronic excessive after load
48
Give 2 causes of increased pre-load, low output chronic HF
- Mitral regurgitation - Fluid overload
49
Give 2 causes of pump failure, low output chronic HF
- Cardiac muscle failure (IHD, cardiomyopathy) - Inadequate HR (beta blockers, post MI)
50
Give 2 causes of chronic excessive after load, low output chronic HF
- Raised BP - Aortic stenosis
51
What is the typical blood gas result of someone with HF?
Metabolic alkalosis with hypokalaemia (due to diuretics)
52
What is the management of chronic HF?
- Aspirin and statin if ischaemic - ACE-In or ARB - BB - MRA (e.g. spironolactone) if significantly reduced LV ejection fraction
53
What are the 2 principles of treating AF?
1. Rate and/or rhythm control 2. Anticoagulation based on CHADSVASc
54
What is the aim of rate control in AF?
To get the HR below 100 bpm to extend the time in diastole and increase the time the ventricles have to fill with blood --> increasing cardiac output
55
What are 3 options for rate control in AF?
1. BB (atenolol) 2. CCB (diltiazem) 3. Digoxin (only in sedentary people)
56
What is the aim of rhythm control in AF
To return the patient to normal sinus rhythm
57
What are the two types of rhythm control of AF? What are used for these?
1. Cardioversion - Electrical - defib under GA - Pharmacological - flecanide 2. Long term rhythm control - BB = first line - Amiodarone
58
What is paroxysmal AF? What is the management?
AF that comes and goes. Still need anticoagulation. Management is usually 'pill in pocket' approach. Flecanide is first line.
59
What CHA2DS2-VASc score indicate anticoagulation?
1 for men 2 for women
60
What scores 2 points in CHADSVASC?
CHA2DS2VASC - Age >75 - Stroke/TIA/VTE
61
What are the options for anticoagulation in AF?
- DOAC - Warfarin
62
When is warfarin contraindicated?
Renal disease
63
What are risk factors for aortic dissection?
- HTN (key) - Trauma - Bicuspid aortic valve - Collagens - Marfan's/Ehlers-Danlos - Turner's/Noonans - Pregnancy - Syphilis
64
What features indicate aortic dissection?
- Chest/back pain - Pulse deficit - weak/absent carotid/brachial/femoral pulse - Variation (>20mmHg) in systolic BP between arms - AR - HTN - Non-specific ECG changes (ST elevation can be seen in inferior leads)
65
What is the Stanford classification for aortic dissection?
- Type A - ascending aorta (2/3rds of cases) - Type B - descending aorta Chest pain is more common in type A and back back is more common in type B
66
What will investigations show in aortic dissection?
- CXR - widened mediastinum - CT angiography of the chest, abdo and pelvis (Ix of choice) - false lumen is a key finding for diagnosis - TOE - used for unstable pts who are too risky to take to CT
67
What is the management of aortic dissection?
- Type A - surgical, BP controlled to 100-120 whilst awaiting intervention - Type B - conservative, bed rest, reduce BP (IV labetalol)
68
What is the normal diameter of the abdominal aorta in females and males? What indicates an aneurysm?
Infrarenal diameters: - Females - 1.5cm - Males - 1.7cm Diameters >3cm = aneurysmal
69
What is the screening for AAA?
A single abdo USS for males >65
70
What are potential outcomes of AAA screening?
- <3 cm - normal - 3-4.4 cm = small aneurysm - rescan every 12 months - 4.5-5.4 cm = medium aneurysm - rescan every 3 months - >5.5 = large aneurysm - refer within 2 weeks to vascular surgery for intervention
71
What is the mortality of a ruptured AAA?
80%
72
What features indicate ruptures AAA?
- Severe central abdo pain radiating to the back - Pulsatile, expansile mass in the abdo - Pts may be shocked/collapsed
73
What is pericarditis?
Inflammation of the pericardium
74
What are the most common causes of pericarditis?
- Idiopathic - Viral infection
75
How does pericarditis present?
- Chest pain (pleuritic, worse on lying down) - Low grade fever
76
What examination finding indicates pericarditis?
Pericardial rub on auscultation - rubbing/scratching sound that occurs alongside HS
77
What would investigations show in pericarditis?
- Raised inflammatory markers - ECG - saddle shaped ST elevation, PR depression - Echo - may show pericardial effusion
78
How do you manage pericarditis?
- NSAIDs - first line - Steroids - second line (recurrent cases/if ass. with inflammatory conditions) Colchicine can be taken for 3 months to reduce the risk of reoccurrence
79
What are complications of pericarditis?
- Pericardial effusion - Cardiac tamponade - Chronic pericarditis
80
What is pericardial effusion?
When the potential space of the pericardial cavity fills with fluid
81
What is cardiac tamponade?
- Where a pericardial effusion is large enough to raise the intra-pericardial pressure - This squeezes the heart and affects its ability to function (decreases CO) - It is an emergency and requires drainage of the pericardial effusion
82
What presentation should make you consider myocarditis?
- Young pt with chest pain - Dyspnoea - Arrhythmias
83
What will investigations show in myocarditis?
- Bloods - raised inflammatory markers, raised cardiac enzymes, raised BNP - ECG - tachy, arrhythmia, ST elevation and T wave inversion
84
What is the management of myocarditis?
- Manage underlying cause e.g. abx if bacterial - Supportive treatment of complications
85
What are complications of myocarditis?
- HF - Arrhythmia - may lead to sudden death - Dilated cardiomyopathy
86
What is the most common valvular heart disease?
AS
87
What are causes of AS?
- Idiopathic age-related calcification (most common) - Bicuspid aortic valve - Rheumatic heart disease
88
What are signs of AS?
- Ejection systolic murmur - Thrill in aortic area - Slow rising pulse - Narrow pulse pressure (difference between systolic and diastolic) - Exertional syncope
89
What is the second most common indication for valve replacement?
MR
90
What are causes of MR?
- Idiopathic weakening of the valve with age - IHD - Infective endocarditis - Rheumatic heart disease - Connective tissue disorders (e.g. Marfan's)
91
What are signs of MR?
- Pan-systolic murmur - Murmur radiates to left axilla - May hear a 3rd HS - Thrill over mitral area - Signs of HF and pulmonary oedema - AF
92
What is malar flush?
- Red discolouration of the skin over the upper cheeks and nose - Due to back pressure of blood into the pulmonary system -> a rise in CO2 and vasodilation
93
What is malar flush associated with?
MS
94
What are the options of valve replacement?
- Bioprosthetic valves - Mechanical valves
95
What are complications of mechanical heart valves?
- Thrombus formation - Infective endocarditis - Haemolysis causing anaemia
96
What do patients with mechanical heart valve require?
- Lifelong anticoagulation with warfarin - INR target = 2.5-3.5 (higher than 2-3 range for AF)
97
What is an issue with bioprosthetic valves?
They have a limited lifespan of around ten years
98
How are valves replaced?
- Open surgery (first line in younger, fitter pts) - Transcatheter Aortic Valve implantation (TAVI)
99
How can the types of cardiomyopathy be classified?
- Primary - predominately affecting heart - Genetic - 2 types, both AD - Mixed - genetic predisposition, triggered by secondary processes - Secondary - infective, toxic, inflammatory causes
100
What is the management of genetic cardiomyopathy?
- Implantable cardioverter-defibrillators are often inserted to reduce the incidence of sudden cardiac death - Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young athletes
101
What are features of postural hypotension?
- Drop in BP >20/10 mmHg within 3 mins of standing (or decrease in systolic BP <90) - Presyncope - Syncope
102
What are treatment options for postural hypotension?
- Midodrine (alpha-adrenergic agonist) - Fludrocortisone
103
How can syncope be classified?
- Reflex - Orthostatic - Cardiac
104
What are the causes of reflex syncope?
- Vasovagal - triggered by emotion, pain, stress ('fainting') - Situational - cough, micturition, GI - Carotid sinus syncope
105
What are causes of cardiac syncope?
- Arrhythmias - bradycardias, tachycardias - Structural - valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy - Other - PE
106
How do you assess someone presenting with syncope?
- History - CVS examination - Postural BP readings - ECG - Other tests will depend on clinical features