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2a > Cardio > Flashcards

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
Q

When should you measure troponin? How do you interpret it?

A

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)
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26
Q

When is a diagnosis of unstable angina given?

A
  • Symptoms of ACS
  • Normal ECG
  • Normal troponin
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27
Q

What is the acute management of MI?

A

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

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28
Q

What are the criteria for PCI in STEMI?

A
  • 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
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29
Q

Was is the FY1 management of NSTEMI?

A
  • Cardiac monitoring
  • Management of complications
  • Load with P2Y12 inhibitor - ticagrelor 180mg
  • Clopidogrel (2nd line)
  • Anticoagulation (fondaparinux)
  • Seek senior help
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30
Q

When is PCI considered in NSTEMI?

A
  • Unstable patients
  • According to their GRACE score (medium/high risk = considered)
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31
Q

What is the GRACE score?

A
  • Gives a 6-month probability of death after having an NSTEMI
  • Above 3% is considered medium to high risk
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32
Q

What meds should be on someones TTO following an MI?

A

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)

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33
Q

What is the FU for an MI?

A
  • Clinic in 1 month
  • TTE if not had as IP
  • Cardiac rehabilitation programme
  • Smoking cessation
  • GP - uptitrate secondary prevention
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34
Q

What advice do you give to pts following an MI?

A
  • 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
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35
Q

Dressler’s syndrome:
1. What is it?
2. How does it present?
3. Investigations
4. Management

A
  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
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36
Q

What happens in acute left ventricular heart failure?

A
  • 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
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37
Q

What are potential triggers of acute LV heart failure?

A
  • 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)
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38
Q

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?

A

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
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39
Q

What signs would indicate acute LV heart failure on examination?

A
  • 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

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40
Q

What can CXR show in acute LV heart failure?

A
  • 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)
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41
Q

What is the initial management of a patient with acute LV heart failure?

A

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

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42
Q

What are the first line and diagnostic investigations for heart failure?

A
  • NT-proBNP
  • Echocardiogram
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43
Q

Other than HF, what issues can cause raised BnP?

A

Sepsis, renal problems, COPD

44
Q

What are poor prognostic factors in HF?

A
  • Smoking
  • Increasing age
  • Low BMI
  • Obesity
  • Diabetes
45
Q

Explain how the causes of chronic HF be classified

A
  • 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
Q

Causes of high output chronic HF

A
  • Hyperthyroidism
  • Anaemia
  • Paget’s disease
  • AV malformation
47
Q

How can low output chronic HF be further classified?

A
  • Increased pre-load
  • Pump failure
  • Chronic excessive after load
48
Q

Give 2 causes of increased pre-load, low output chronic HF

A
  • Mitral regurgitation
  • Fluid overload
49
Q

Give 2 causes of pump failure, low output chronic HF

A
  • Cardiac muscle failure (IHD, cardiomyopathy)
  • Inadequate HR (beta blockers, post MI)
50
Q

Give 2 causes of chronic excessive after load, low output chronic HF

A
  • Raised BP
  • Aortic stenosis
51
Q

What is the typical blood gas result of someone with HF?

A

Metabolic alkalosis with hypokalaemia (due to diuretics)

52
Q

What is the management of chronic HF?

A
  • Aspirin and statin if ischaemic
  • ACE-In or ARB
  • BB
  • MRA (e.g. spironolactone) if significantly reduced LV ejection fraction
53
Q

What are the 2 principles of treating AF?

A
  1. Rate and/or rhythm control
  2. Anticoagulation based on CHADSVASc
54
Q

What is the aim of rate control in AF?

A

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
Q

What are 3 options for rate control in AF?

A
  1. BB (atenolol)
  2. CCB (diltiazem)
  3. Digoxin (only in sedentary people)
56
Q

What is the aim of rhythm control in AF

A

To return the patient to normal sinus rhythm

57
Q

What are the two types of rhythm control of AF? What are used for these?

A
  1. Cardioversion
    • Electrical - defib under GA
    • Pharmacological - flecanide
  2. Long term rhythm control
    • BB = first line
    • Amiodarone
58
Q

What is paroxysmal AF? What is the management?

A

AF that comes and goes. Still need anticoagulation. Management is usually ‘pill in pocket’ approach. Flecanide is first line.

59
Q

What CHA2DS2-VASc score indicate anticoagulation?

A

1 for men
2 for women

60
Q

What scores 2 points in CHADSVASC?

A

CHA2DS2VASC
- Age >75
- Stroke/TIA/VTE

61
Q

What are the options for anticoagulation in AF?

A
  • DOAC
  • Warfarin
62
Q

When is warfarin contraindicated?

A

Renal disease

63
Q

What are risk factors for aortic dissection?

A
  • HTN (key)
  • Trauma
  • Bicuspid aortic valve
  • Collagens - Marfan’s/Ehlers-Danlos
  • Turner’s/Noonans
  • Pregnancy
  • Syphilis
64
Q

What features indicate aortic dissection?

A
  • 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
Q

What is the Stanford classification for aortic dissection?

A
  • 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
Q

What will investigations show in aortic dissection?

A
  • 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
Q

What is the management of aortic dissection?

A
  • Type A - surgical, BP controlled to 100-120 whilst awaiting intervention
  • Type B - conservative, bed rest, reduce BP (IV labetalol)
68
Q

What is the normal diameter of the abdominal aorta in females and males? What indicates an aneurysm?

A

Infrarenal diameters:
- Females - 1.5cm
- Males - 1.7cm

Diameters >3cm = aneurysmal

69
Q

What is the screening for AAA?

A

A single abdo USS for males >65

70
Q

What are potential outcomes of AAA screening?

A
  • <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
Q

What is the mortality of a ruptured AAA?

A

80%

72
Q

What features indicate ruptures AAA?

A
  • Severe central abdo pain radiating to the back
  • Pulsatile, expansile mass in the abdo
  • Pts may be shocked/collapsed
73
Q

What is pericarditis?

A

Inflammation of the pericardium

74
Q

What are the most common causes of pericarditis?

A
  • Idiopathic
  • Viral infection
75
Q

How does pericarditis present?

A
  • Chest pain (pleuritic, worse on lying down)
  • Low grade fever
76
Q

What examination finding indicates pericarditis?

A

Pericardial rub on auscultation - rubbing/scratching sound that occurs alongside HS

77
Q

What would investigations show in pericarditis?

A
  • Raised inflammatory markers
  • ECG - saddle shaped ST elevation, PR depression
  • Echo - may show pericardial effusion
78
Q

How do you manage pericarditis?

A
  • 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
Q

What are complications of pericarditis?

A
  • Pericardial effusion
  • Cardiac tamponade
  • Chronic pericarditis
80
Q

What is pericardial effusion?

A

When the potential space of the pericardial cavity fills with fluid

81
Q

What is cardiac tamponade?

A
  • 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
Q

What presentation should make you consider myocarditis?

A
  • Young pt with chest pain
  • Dyspnoea
  • Arrhythmias
83
Q

What will investigations show in myocarditis?

A
  • Bloods - raised inflammatory markers, raised cardiac enzymes, raised BNP
  • ECG - tachy, arrhythmia, ST elevation and T wave inversion
84
Q

What is the management of myocarditis?

A
  • Manage underlying cause e.g. abx if bacterial
  • Supportive treatment of complications
85
Q

What are complications of myocarditis?

A
  • HF
  • Arrhythmia - may lead to sudden death
  • Dilated cardiomyopathy
86
Q

What is the most common valvular heart disease?

A

AS

87
Q

What are causes of AS?

A
  • Idiopathic age-related calcification (most common)
  • Bicuspid aortic valve
  • Rheumatic heart disease
88
Q

What are signs of AS?

A
  • Ejection systolic murmur
  • Thrill in aortic area
  • Slow rising pulse
  • Narrow pulse pressure (difference between systolic and diastolic)
  • Exertional syncope
89
Q

What is the second most common indication for valve replacement?

A

MR

90
Q

What are causes of MR?

A
  • Idiopathic weakening of the valve with age
  • IHD
  • Infective endocarditis
  • Rheumatic heart disease
  • Connective tissue disorders (e.g. Marfan’s)
91
Q

What are signs of MR?

A
  • 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
Q

What is malar flush?

A
  • 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
Q

What is malar flush associated with?

A

MS

94
Q

What are the options of valve replacement?

A
  • Bioprosthetic valves
  • Mechanical valves
95
Q

What are complications of mechanical heart valves?

A
  • Thrombus formation
  • Infective endocarditis
  • Haemolysis causing anaemia
96
Q

What do patients with mechanical heart valve require?

A
  • Lifelong anticoagulation with warfarin
  • INR target = 2.5-3.5 (higher than 2-3 range for AF)
97
Q

What is an issue with bioprosthetic valves?

A

They have a limited lifespan of around ten years

98
Q

How are valves replaced?

A
  • Open surgery (first line in younger, fitter pts)
  • Transcatheter Aortic Valve implantation (TAVI)
99
Q

How can the types of cardiomyopathy be classified?

A
  • Primary - predominately affecting heart
  • Genetic - 2 types, both AD
  • Mixed - genetic predisposition, triggered by secondary processes
  • Secondary - infective, toxic, inflammatory causes
100
Q

What is the management of genetic cardiomyopathy?

A
  • 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
Q

What are features of postural hypotension?

A
  • Drop in BP >20/10 mmHg within 3 mins of standing (or decrease in systolic BP <90)
  • Presyncope
  • Syncope
102
Q

What are treatment options for postural hypotension?

A
  • Midodrine (alpha-adrenergic agonist)
  • Fludrocortisone
103
Q

How can syncope be classified?

A
  • Reflex
  • Orthostatic
  • Cardiac
104
Q

What are the causes of reflex syncope?

A
  • Vasovagal - triggered by emotion, pain, stress (‘fainting’)
  • Situational - cough, micturition, GI
  • Carotid sinus syncope
105
Q

What are causes of cardiac syncope?

A
  • Arrhythmias - bradycardias, tachycardias
  • Structural - valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
  • Other - PE
106
Q

How do you assess someone presenting with syncope?

A
  • History
  • CVS examination
  • Postural BP readings
  • ECG
  • Other tests will depend on clinical features

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