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Finals > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are some key differentials for acute chest pain?

A 
MI
PE
Aortic Dissection
Pericarditis
Pneumothorax
Trauma
Panic attack
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2
Q

What are some differentials for subacute chest pain?

A 
Sick cell crisis
Cardiac tamponade
Aortic aneurysm
HOCM
Myocarditis
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3
Q

What are some chronic causes of chest pain?

A 
Angina
Pneumonia
Aortic stenosis
Referred pain from GI tract
Neoplasms
Congenital heart defects
Arrhythmia
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4
Q

What can cause palpitations?

A 
Arrhythmia
Septal defects
Cardiomyopathy
Congestive heart failure
Mitral valve prolapse
Valvular Disease
Anaemia
Electrolyte imbalance
Hyperthyroid
Hypoglycaemia
Hypovolaemia
Phaeochromocytoma

Drugs - alcohol, caffeine, tobacco, prescription etc.
Anxiety

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5
Q

What is syncope? (what 3 things must it be)

A

Transient

Loss of consciousness

Due to global cerebral hypoperfusion (typically hypotension)

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6
Q

What key things do you want to know in a syncope history

A

5P’s and 5C’s

Prodrome
Precipitant
Palpitation
Position
Post event
Colour
Convulsions
Continence
Cardiac hx
Cardiac FH of sudden death
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7
Q

What are the types of syncope?

A

Neurally mediated
Postural
Arrhythmia induced
Structural

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8
Q

What is neurally mediated syncope and what are the types?

A

Inappropriate autonomic response to a trigger

Vasovagal
Situational
Carotid sinus hypersensitivity

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9
Q

What is postural syncope?

A

Happen due to insufficient barereceptor response to standing up. Due to:

  • Autonomic failure secondary to drugs
  • Hypovolaemia
  • Primary autonomic failure - Parkinson’s/lewy body
  • Secondary autonomic failure - diabetes, uraemia, spinal cord lesions
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10
Q

What is structural syncope?

A

Mechanical obstruction to LV inflow or outflow meaning systemic vasculature can’t compensate to exercise. Causes include:

  • Valvular - aortic stenosis
  • Mass - atrial myxoma
  • HOCM
  • Constrictive pericarditis
  • Non-cardiac - PE/aortic dissection
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11
Q

Give some causes for limb pain and swelling? (VITAMIN D)

A

Vascular - DVT, varicose veins, IVC obstruction, PVD, congestive heart failure

Infection/inflammation - cellulitis, septic arthritis, osteomyelitis

Trauma - compartment syndrome, rhabdo,

Autoimmune - rheumatoid

Metabolic - gout, vit D deficiency, hypoproteinaemia

Multiple - lymphoedema, bakers cyst, AKI/CKD

Neoplasms

Drugs - statins, calcium blockers, NSAIDs

Degenerative - Osteoarthritis

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12
Q

What is type 1 heart block

A 
PR >0.2s
Regular
Not dangerous itself but can indicate pathology:
- coronary artery disease
- digoxin poisoning
- electrolyte disturbance
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13
Q

What are the types of 2nd degree heart block?

A

Mobitz type 1:

  • PR interval progressively increase until one is dropped
  • cyclical
  • Not dangerous but can indicate pathology

Mobitz type 2:

  • Normal PR constant
  • Cyclically drop QRS
  • Can lead to complete heart block
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14
Q

What is type 3 heart block?

A

Atrial contraction normal but not conducted to ventricles

Can occur acutely after MI or also due to bundle of his fibrosis

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15
Q

What are the features of a complete heart block?

A
  • QRS rate slow 36bpm - bradycardia
  • p wave rate normal
  • no relationship between p and QRS
  • Wide QRS
  • Syncope
  • Heart failure
  • Wide pulse pressure
  • JVP - cannon wave
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16
Q

What are some indications for temporary pacemakers?

A

Symptomatic/haemodynamically unstable bradycardia not responding to atropine

Post anterior MI - type 2 or complete heart block

Trifascicular block prior to surgery

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17
Q

What is a bi/trifascicular heart block?

A

Bifascicular block:
- RBBB + Left anterior or posterior fascicle block
= RBBB + Left/Right axis deviation

Trifascicular block:
- RBBB + left/right axis deviation + first degree heart block

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18
Q

What happens in a bundle branch block?

A

Depolarisation reach inter ventricular septum but spread across septum is altered:

  • Normal PR
  • Wide QRS
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19
Q

How do left and right bundle branch blocks appear?

A

WilliaM MarroW

Left = W in V1, M in V6
Right = M in V1 W in V6

Newfound LBBB with chest pain may indicate MI or aortic stenosis

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20
Q

Which factors would make rate control more appropriate for AF?

A

Older than 65

Hx of ischaemic heart disease

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21
Q

Which factors would make rhythm control appropriate for AF?

A 
<65yo
Symptomatic
First presentation
Lone AF or secondary to corrected precipitant
Congestive heart failure
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22
Q

How long should a patient be anti coagulated for before treatment for AF?

A

4 weeks

Can do treatment immediately if echo done to confirm no thrombus present (emergency)

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23
Q

Give some key complications of catheter ablation in AF?

A

Cardiac tamponade
Stroke
Pulmonary valve stenosis

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24
Q

When is cardioversion considered in AF?

A

Haemodynamically unstable

Haemodynamically stable but rhythm control preferred

Anticoagulate for 4 weeks after cardioversion

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25
Q

What time period is used to determine whether cardioversion is considered?

A

<48 hr - heparinise and DC cardiovert or chemical cardiovert

> 48h - >3wk anticoagulation or TOE to confirm no thrombus

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26
Q

What would make a patient a high risk of cardioversion failure? What should be done?

A

Previous failure
AF recurrence

> 4 wks amiodarone or sotalol before DC cardioversion

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27
Q

What is Wolf Parkinson White?

A

Accessory bundles form a direct connection from the atria to the ventricles

There is no AVN to delate condition meaning there is early pre-excitation of the ventricles

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28
Q

How does WPW appear on ECG?

A 
Sinus rhythm
Short PR
Delta wave on QRS - slurred upstroke
Short QRS
Right/Left axis deviation
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29
Q

What is WPW associated with?

A 
HOCM
Mitral valve prolapse
Ebsteins anomoly 
Thyrotoxicosis
Secundum ASD
Paroxysmal tachycardia - can lead to VT and VF
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30
Q

How is WPW managed

A

Ablation of accessory pathway

Medical - Sotalol, amiodarone, flecainide

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31
Q

Why should sotalol be avoided in WPW if a patient also has AF?

A

Increased risk of VF

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32
Q

How is angina managed?

A

Aspirin + statin + GTN for all

  1. CCB (diltiazem or verapamil) or BB
  2. CCB (MR nifedipine) and BB
  3. add isosorbide nitrate or ivabradine or nicorandil
  4. CABG or PCI
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33
Q

What nitrate free time is recommended for patients with nitrate tolerance?

A

10-14 hours a day

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34
Q

What are the signs and symptoms of ACS?

A 
Central crushing chest pain
SOB
sweating, pale and clammy 
Palpitations and tachycardia 
N&V
pulmonary oedema = lung crepitations
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35
Q

What ECG changes define STEMI?

What are the timings for some other ECG changes?

A

ST elevation:
>2mm in 2 contiguous chest leads
<1mm in 2 contiguous limb leads

New LBBB

within minutes: hyperacute T (tall)
within 12 hours: Pathological Q waves (>25% height of R)
within days: T wave inversion

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36
Q

What complications are associated with STEMI’s? State the timings of these if they are significant

A

Heart block (particularly after inferior)
Arrest - VF/pVT
Cardiogenic shock
HF
Pericarditis (48hrs)
Dressler’s syndrome (4 weeks)
LV aneurysm can lead to stroke
LV wall rupture leading to tamponade (1 week)
VSD
Mitral regurgitation leading to flash pulmonary oedema

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37
Q

What immediate management is required for ?ACS

A 
Morphine - 10mg IV
Oxygen (if sats <94% on air)
Nitrates (if no bradycardia/BP<90)
Aspirin 300mg
Clopidogrel 300/600mg

Anti-emetic - 10mg IV Metoclopramide

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38
Q

What is the long term management for an MI?

A

Lifestyle: stop smoking, drinking, good diet, exercise

Aspirin 75mg daily
Clopidogrel/Ticagrelor/Prasugrel
Statin
Beta blocker
ACEi

+ eplerenone if HF or LV dysfunction

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39
Q

What are poor prognostic indicators for ACS?

A

Arrest at presentation
Hypotensive
Raised cardiac markers
Raised creatinine

High Killip class: 
I - No signs of heart failure
II - Lung crackles, S3
III - Frank pulmonary oedema
IV - Cardiogenic shock
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40
Q

What are the main causes of mitral regurgitation?

A

PRIMARY: degenerative, rheumatic fever, infective endocarditis, Marfans

SECONDARY (valve incompetent due to heart disortion): dilated cardiomyopathy, post MI ischaemic cardiomyopathy, HF

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41
Q

What are the causes of acute mitral regurgitation and how does it present?

A

Infective endocarditis and post MI ischaemic cardiomyopathy

Flash pulmonary oedema causing dyspnoea and shock
This is because no time for remodelling so blood backs up

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42
Q

What are the signs and symptoms of mitral regurgitation?

A 
Pansystolic murmur radiating to the axilla
Soft blowing
Quite S1 (not shutting)
Split S2 (severe)
S3 (blood rush in to dilated ventricle)
Displaced apex beat + heave

LV failure: fatigue, orthopnoea, pulmonary oedema

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43
Q

What investigations would you request for mitral regurgitation and what may they show?

A

ECG - bifid, broad p - enlarged atria

CXR - cardiomegaly, double R heart border, pulmonary oedema

Transoesophageal echo - diagnose/determine severity

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44
Q

How is mitral regurgitation managed?

A

Acute - nitrates, diuretics, positive inotropes and balloon pump
HF - ACEi +- B Blockers and spironolactone

Acute severe - surgical valvuloplasty/valve replacement

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45
Q

What are the common causes of aortic regurgitation?

A

Valve disease:

  • Rheumatic fever
  • Infective endocarditis
  • Connective tissue disorders
  • Bicuspid aortic valve

Aortic root disease:

  • Aortic dissection
  • Marfans
  • Ank spond
  • Syphilis
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46
Q

What are the signs associated with aortic regurgitation?

A 
Early diastolic murmur (sitting forward, on expiration)
Collapsing pulse - corrigan's
Wide pulse pressure
Quincke's sign - nailed pulsing
De Musset's sign - head bobbing
Traube's sign - pistol shot femoral
Gerhardt - splenic pulsation

Mid diastolic Austin flint murmur in severe AR

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47
Q

How is aortic regurgitation investigated?

A

CXR - cardiomegaly, dilated ascending aorta, pulmonary oedema

ECG - LVH so deep S in V1/2 and tall R in V5/6

Echo - diagnostic

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48
Q

How is aortic regurg managed?

A

Reduce hypertension - ACEi
Regular echo - monitor
Surgery - indications:
- severe AR with enlarged ascending aorta
- increasing symptoms
- deteriorating LV function
- infective endocarditis refractory to medical therapy

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49
Q

What symptoms can aortic regurgitation present with?

What could cause an acute presentation and what would be the key symptoms?

A 
Exertional dyspnoea
Orthopnoea
PND
Palpitations
Angina
Syncope

ACUTE:

  • infective endocarditis and aortic dissection
  • dyspnoea (pulmonary oedema)
  • angina (reduced coronary filling due to regurg during diastole)
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50
Q

What is aortic stenosis caused by?

A

Elderly - calcification of aortic valve - check for corneal arcus

Congenital - bicuspid aortic valve, William’s syndrome

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51
Q

What signs are associated with aortic stenosis?

A

Crescendo-decrescendo ejection systolic murmur radiating to carotids
Slow rising pulse
Narrow pulse pressure
Heave

Soft S2 and presence of S4 in severe

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52
Q

What investigations would you request for aortic stenosis?

A

ECG - LVH (deep S in V1/2 and tall R in V5/6) left ventricular strain, LBBB, poor r wave progression

CXR - calcifications, cardiomegaly

Echo - estimate pressures and assess degree of disease

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53
Q

What are the main symptoms of aortic stenosis?

A

SAD:

  • syncope
  • angina (hypertrophies muscle has high O2 demand)
  • dyspnoea (L HF due to hypertrophy eventually causing impaired relaxation and diastolic dysfunction)
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54
Q

How is aortic stenosis managed?

A

Asymptomatic - observe

Symptomatic - valve replacement

Can consider surgery in asymptomatic + >40mmHg valvular gradient

Balloon valvuloplasty for those with critical AS but not fit for replacement

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55
Q

What are the main complications associated with aortic stenosis?

A

Congestive heart failure
Infective endocarditis
Emboli

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56
Q

What are the advantages of each valve type?

A

Bioprosthetic - req. replacing but don’t need anticoagulant

Metallic - last lifetime but anticoag and make loud clicking noise

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57
Q

How can mitral stenosis present? What is the pathophysiology behind this?

A

Increased LA pressure means it dilates:

  • AF
  • Stroke due to thrombi

Increased pressure within the pulmonary system:
- RV failure (peripheral oedema, ascites, hepatomegaly, raised JVP, dyspnoea, reduced exercise tolerance)

Enlarged LA can compress with L recurrent laryngeal nerve
- hoarse voice

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58
Q

What are the examination findings in mitral stenosis?

A

Mid to late diastolic murmur - expiration, left side, with bell
Loud S1 - opening snap
Low volume pulse
Malar flush

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59
Q

What causes mitral stenosis?

A

RHEUMATIC FEVER

Others:

  • calcification
  • congenital
  • carcinoid disease
  • SLE
  • infective endocarditis
  • Rheumatoid arthritis
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60
Q

What investigations are done for mitral stenosis?

A

CXR - Cardiomegaly with double R heart border, prominent pulmonary vessels, valve calcification

ECG - AF, broad bifid P due to LA enlargement

Echo - assess level of stenosis

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61
Q

How is mitral stenosis managed?

A

Percutaneous mitral commissurotomy (PMC) which is balloon dilation

Manage medical symptoms with diuretics, nitrates, B blockers, Ca channel blockers

Anticoagulate for AF

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62
Q

Which murmurs are systolic?

A

ASMR

Aortic Stenosis
Mitral Regurg

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63
Q

What are the most common causes of acute vs chronic heart failure?

A

ACUTE: ACS, arrhythmia, valve pathology, tamponade

CHRONIC: HTN, IHD, cardiomyopathy (dilated/hypertrophic) valve (stenosis/regurg), AF, CHD

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64
Q

What are the key signs and symptoms of acute Heart Failure?

A

Breathlessness
Oedema
Fatigue
Reduced exercise tolerance

Cyanosis
Tachycardia
Raised JVP
Displaced apex beat
Chest signs - wheeze and bibasal crackles
S3 heart sound
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65
Q

What is high output heart failure and what are some causes?

A

Cardiac output sufficient but increased metabolic demand, reduced O2 carrying ability, or reduced TPR

  • anaemia
  • thyrotoxicosis
  • sepsis
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66
Q

What physiological responses cause heart failure to worsen?

A

Increased total peripheral resistance - this increases afterload and strain on heart

Increased HR - increased workload of heart - higher O2 demand

Increased blood volume - ventricles dilate, decrease contractility, increase oedema

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67
Q

What is the New York heart failure classification?

A

1 - No symptoms at rest or limitations to daily activities
2 - slight limitation to physical activity
3 - considerable limitation to physical activity
4 - symptoms at rest

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68
Q

What are the key signs and symptoms of chronic heart failure?

A
  • Dyspnoea
  • Fatigue with reduced exercise tolerance
  • Oedema

Pink frothy sputum, wheeze and bibasal crepitations
Orthopnoea and PND
Displaced apex beat
Tachycardic

Right side/congestive - peripheral oedema, raised JVP, hepatomegaly, ascites, nocturia

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69
Q

How is heart failure managed acutely?

A
  1. IV furosemide - 40mg
  2. If this fails try CPAP

+ oxygen
+ opioids to reduce anxiety and help dyspnoea

+/- Vasodilators
+/- Inotropic agents
+/- Ultrafiltration
+/- Intra-aortic balloon pump

Consider short term stopping of beta blockers

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70
Q

How is HF-REF managed?

A

ACEi and Beta blockers

Add spironolactone or alpha blocker (K+ <>4.5)

3rd line = specialist
- ivabradine, valsartan, hydralyzine + nitrate, digoxin and cardiac resynchronisation

One off pneumococcal vaccine - booster if asplenic, CKD or splenic dysfunction
Yearly influenze vaccine
Cardiorespiratory rehabilitation exercises
Antiplatelet and statin considered

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71
Q

When is ivabradine used in heart failure management?

A

Sinus rhythm >75 bpm

Ejection fraction <35%

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72
Q

When is sacubitril-valsartan used in heart failure management?

A

Ejection fraction <35%
Symptomatic on ACEi and Beta blocker

Start after ACEi/ARB washout period

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73
Q

When is digoxin used in heart failure management?

A

Used for symptomatic relief due to inotropic effects

Used in concurrent AF

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74
Q

When is Hydralyzine + nitrate used in heart failure management?

A

Esp. afro-caribbean patients

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75
Q

When is cardiac resynchronisation used in heart failure?

A

Widened QRS on ECG

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76
Q

How is heart failure investigated?

A
  1. B type natriuretic peptide and ECG (?cause)
  2. Transthoracic Echo

+CXR
+ find cause (BP, coronary angio, FBC, TFT)

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77
Q

What are the stages of hypertension?

A

Stage 1 - clinic >140/90 or ambulatory >135/85
Stage 2 - clinic >160/100 or ambulatory >150/95
Stage 3 - clinic >180/120

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78
Q

What is indicative of white coat hypertension?

A

Drop in systolic BP >20mmHg or diastolic >10

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79
Q

How is hypertension investigated?

A

Clinic BP >140/90 = ABPM (2/hr) or HBPM (2/day)

Glucose ?diabetes
Urine dip ?proteinuria
Bloods ?renal disease ?cholesterol

If age <40 refer for specialist investigation
If BP >180/120 then refer for immediate assessment

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80
Q

When should drug treatment be offered for hypertension?

A

Stage 1 and <80 and 1 of

  • end organ damage
  • CVS disease
  • Renal disease
  • QRISK >10%
  • diabetes

Stage 2 and above

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81
Q

What drug treatment is offered for hypertension?

A

<55 or T2DM:

  1. A
  2. A + C/D

> 55 or afro-Caribbean:

  1. C
  2. C + A (ARB if afro-caribbean)
  3. A+C+D
  4. Spironolactone (if K<4.5) or A/B blocker (if K<4.5)

A - ACEi or Angiotensin 2 antagonist
C - Ca2+ blocker
D - thiazide diuretic

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82
Q

What lifestyle advice is given for HTN?

A 
Reduce salt intake
Reduce caffeine intake
Stop smoking
Stop drinking alcohol 
Exercise
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83
Q

What is the target blood pressure for those being treated for hypertension?

A

Age <80:
Clinic <140/90 or ABPM <135/85

Age>80:
Clinic <150/90 or ABPM <145/85

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84
Q

What signs do you look for on examination in hyperlipidaemia?

A 
Corneal arcus
Tendon xanthoma (often achilles)
Palmar xanthoma 
Eruptive xanthoma (red/yellow vesicles on extensors)
Xanthelasma - yellow around eyelids
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85
Q

How is xanthelasma managed?

A

Surgical removal
Laser therapy
topical trichloroacetic acid

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86
Q

What are the secondary causes of hyperlipidaemia? Which cause predominantly high cholesterol vs high triglycerides

A

Cholesterol:

  • Hypothyroid
  • Obstructive jaundice
  • Nephrotic syndrome

Triglycerides:

  • Diabetes
  • Obesity
  • Alcohol
  • CKD
  • Drugs (COCP, thiazides, b-blockers)
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87
Q

When is a) primary and b) secondary prevention of hyperlipidaemia required and what is given?

A

a) 20mg atorvastatin
- 10 year CVS risk >10%, T1DM, CKD with eGFR <60

b) 80mg atorvastatin
- IHD, PAD, cerebrovascular disease

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88
Q

What is the spectrum of peripheral vascular disease? What are the signs and symptoms associated?

A

Intermittent claudication - LL pain on exercise

Critical limb ischaemia - rest pain >2wks/gangrene/ulceration.

Pale and cold leg with lack of hair and skin changes

Weak/absent pulses

89
Q

How is critical limb ischaemia defined?

A 
1+ of:
- Pain at rest for >2 weeks
- Gangrene
- Ulceration
ABPI <0.5 indicative
90
Q

How would you investigate peripheral vascular disease?

A

Hx and exam (smoking and diabetes)
CVS assessment - BP, FBC, lipids, BM, ECG

Duplex ultrasound first line
ABPI

MRA before intervention

91
Q

How is peripheral vascular disease managed?

A

Modify CVS risk factors and exercise training
Atorvastatin 80mg
Clopidogrel

Revascularisation - angiography, stent or bypass
Amputation if others not suitable

Naftidrofuryl oxalate - vasodilator - symptom control if surgery not wanted

92
Q

How can ankle brachial pressure index be interpreted?

A 
>1.4 = suspect PAD especially if diabetic 
0.9-1 = normal
0.6-0.9 = Claudication
0.3-0.6 = rest pain
<0.3 = impending

<0.5 = critical limb ischaemia

93
Q

What are the features of acute limb ischaemia?

A

6P’s

Pale
Pulseless
Perishingly cold
Paraesthesia
Pain
Paralysed
94
Q

Where can peripheral vascular disease affect in the upper limb?

A

Subclavian artery

Brachiocephalic trunk

95
Q

What are the features of upper limb peripheral vascular disease?

A

Subclavian steal syndrome: arm claudication and neurological sequalae (syncope)

Can get the 6 P’s as per lower limb

96
Q

What are the types of shock?

A

Hypovolaemic
Distributive - e.g. septic, anaphylactic
Cardiogenic - ventricles unable to empty
Mechanical - ventricles unable to fill

97
Q

What is mitral valve prolapse associated with?

A 
Congenital heart disease - PDA, ASD
Turner's
Marfans and Ehler's Danlos
PCKD
WPW and Long QT
98
Q

What murmur is heard in mitral valve prolapse?

A

Mid systolic click (late systolic when patient squatting)

Late systolic murmur (longer when patient standing)

99
Q

What are the symptoms of mitral valve prolapse?

A 
Atypical chest pain
Palpitations 
\+/- Fatigue
\+/- SOB
\+/- Dizziness
100
Q

What complications are associated with mitral valve prolapse?

A

Mitral regurg
Arrhythmia (Long QT)
Emboli - stroke
Sudden death

101
Q

How is mitral valve prolapse managed?

A

Low risk - nothing
High risk of emboli - anticoagulate
Palpitations/symptoms - beta blockers
Risk of mitral regurgitation - replace valve

102
Q

Where does infective endocarditis commonly affect?

A

Left sided valves - mitral most common

IVDU - tricuspid

103
Q

What are the risk factors for infective endocarditis?

What else can cause endocarditis?

A 
Rheumatic fever
IVDU
Prosthetic valves
Poor oral hygiene/dental procedures
New piercing 
Congenital heart disease

Non-infective (SLE and malignancy)

104
Q

How does infective endocarditis present acutely?

A

Fever + new murmur = IE unless proven otherwise

Heart failure (SOB and orthopnoea) 
Stroke/TIA/PE
105
Q

What criteria is used for diagnosing infective endocarditis? Briefly overview what is in it

A

Modified Dukes
Pathological
- +ve microbiology on specimen of tissue

Major

  • +ve blood cultures
  • echo (oscillating structures, abscess, valve regurg, dehiscence of prosthetic valve)

Minor

  • fever >38
  • pre-existing heart condition or IVDU
  • vascular signs (Janeway, petechiae, splinter haemorrhages, splenomegaly)
  • immunological signs (Oslers, Roth spots, glomerulonephritis)
106
Q

Which organisms typically cause infective endocarditis?

A

Staph aureus in general population and IVDU

Staph epidermidis if <2 months post prosthetic valve surgery

Strep viridian’s in developing countries and poor dental hygiene

Strep Bovis in colorectal cancer

107
Q

What are the poor prognostic factors for infective endocarditis?

A

Staph aureus infection

Early prosthetic valve infection

Culture negative endocarditis

Low complement levels

108
Q

How is infective endocarditis managed immediately? i.e. with no culture results

A

Blind:
Native: Amoxicillin (vancomycin if allergic) + gent
Prosthetic: Vancomycin + rifampicin + gentamicin
Severe sepsis: Vancomycin and gentamicin

109
Q

How is infective endocarditis managed in native valves once culture results are back?

A

Staph - fluclox
Strep - Benzylpenicillin (+low dose gent if less sensitive i.e. not viridans)

Vanc+rifampicin if allergic/MRSA
Vanc if strep and allergic

110
Q

How is infective endocarditis managed in prosthetic valves?

A

Flucloxacillin + Rifampicin + low dose gentamycin

vancomycin if allergic or MRSA

111
Q

What are the indications for surgery in infective endocarditis?

A 
Severe valve incompetence
Aortic abscess
Resistant infections/fungal
Cardiac failure
Recurrent emboli
112
Q

How would you know someone with infective endocarditis had developed an aortic abscess?

A

Prolonged PR on ECG

113
Q

When is antibiotic prophylaxis recommended for infective endocarditis?

A

At risk and already receiving Abx for GI/genitourinary surgery

Not routinely recommended anymore - dental, GI, genitourinary or respiratory tract surgery

114
Q

What can cause pericarditis?

A 
Infection - normally viral (coxackie B) or TB
Post MI - Dressler's syndrome
Trauma
!!Malignancy!!
Uraemia
115
Q

How does pericarditis present?

A

Need 2/4 of:
Pleuritic chest pain - Relieved by sitting forward
Pleural effusion
Pericardial friction rub
ECG changes (PR depression and ST elevation)

\+/-
Fever
Tachycardia and tachypnoea
SOB
Dry cough
116
Q

What investigations are done for pericarditis?

A

ECG - widespread saddle ST elevation, PR depression, t wave invesion

Transoesophageal echo

117
Q

How is pericarditis managed?

A

NSAID’s and Colchicine for idiopathic and viral
Fix the cause
Supportive care

118
Q

What complications are associated with pericarditis?

A

Pericardial thickening –> constrictive pericarditis

119
Q

What is Dressler’s syndrome?

A

Autoimmune reaction to antigenic proteins formed in myocardial recovery post MI

2-6 weeks post MI –> pericarditis

Fever, pleuritic pain, pericardial effusion, raised ESR

120
Q

What are the signs and investigation results of a pericardial effusion?

A

Soft distant heart sounds
Apex beat obscured
Friction run which disappear over time

CXR - enlarged heart with precise outlines
ECG - low voltage QRS
Echo - shows the effusion

121
Q

What commonly causes constrictive pericarditis?

A

TB induced pericarditis

122
Q

How does constrictive pericarditis present?

What is seen on CXR?

A

Dyspnoea
Right heart failure - raised JVP, ascites, oedema, hepatomegaly
Loud S3
Kussmaul’s sign - paradoxical JVP rise on inspiration

Pericardial calcification

123
Q

Compare the JVP waveform in constrictive pericarditis vs tamponade

A

X and Y descent are both present in constrictive pericarditis however in tamponade there is no Y descent (Y descent represents ventricle filling in diastole)

124
Q

What is cardiac tamponade caused by?

A

Trauma
Pericarditis
Malignancy
Iatrogenic

125
Q

What should be done if you suspect cardiac tamponade?

A

FAST scan and bedside echo ASAP

  • ECG
  • Transthoracic echo
  • CXR
  • FBC
  • ESR
  • Troponin
126
Q

How is a cardiac tamponade managed? (Stable vs unstable)

A

If haemodynamically stable/pre-tamponade - NSAIDs + gastroprotection

Haemodynamically unstable:
Needle pericardiocentesis - rarely works
Clamshell thoracotomy

127
Q

Where is the needle inserted in a pericardiocentesis?

A

Angle of xiphisternum with L rib border

Aim towards left scapula

128
Q

What are the classical triad of features of cardiac tamponade?

A

Beck’s Triad:

  • Hypotension
  • Raised JVP
  • Muffled heart sounds
129
Q

What other features are seen in cardiac tamponade? Including ECG findings

A

Pulsus paradoxus - BP drop on inspiration
Dysnpnoea
Tachycardia

Electrical alternans on ECG - alternating QRS amplitude

130
Q

What happens in an aortic dissection?

A

Tear in the tunica intima of the wall of the aorta

131
Q

How does an aortic dissection present?

A

Tearing pain that goes through to the back

Pulse deficit - weak/absent carotid, radial or femoral

Aortic regurg

Hypertension

132
Q

What are the types of aortic dissection?

A

Stanford Classification
A - Ascending aorta
B - Descending aorta

DeBakey classification
I - Ascending aorta –> arch and slightly distal
II - Originate and confined to ascending aorta
III - Originate descending, extend distally

133
Q

How can aortic dissections be investigated?

A

Guided by presentation - often acute

CT CAP ideal - stable and awaiting surgery
TOE - For unstable
CXR - widened mediastinum

134
Q

How are aortic dissections managed?

A

Type A - Surgery
BP <100-120 whilst waiting

Type B - Conservative/bed rest
IV labetalol

135
Q

What are the complications associated with an aortic dissection?

A

Backward tear:

  • Aortic regurg/incompetence
  • MI - typically inferior

Forward tear:

  • Unequal arm pulses
  • Renal failure
  • Stroke
136
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Inherited condition presenting with syncope, palpitations or sudden cardiac death

Autosomal dominant

RV myometrium replaced with fatty/fibrofatty tissue

137
Q

How is arrhythmogenic right ventricular cardiomyopathy investigated?

A

ECG - V1-3 t wave inversion. Epsilon wave on QRS

Echo - subtle to start. Enlarged hypo kinetic RV

MRI - show fibrofatty tissue

138
Q

How is arrhythmogenic right ventricular cardiomyopathy managed?

A

Sotalol
Catheter ablation - prevent ventricular tachy
ICD

139
Q

What is Naxos disease?

A

Autosomal recessive variant of arrhythmogenic RV cardiomyopathy

Triad: ARVC, palmoplantar keratosis, woolly hair

140
Q

How is atrial fibrillation managed post stroke?

A

Warfarin or direct thrombin/factor Xa inhibitor

2 weeks post if no haemorrhage

141
Q

What is an atrial myxoma?

A

Cardiac tumour in LA
Common in females

  • Dyspnoea, fatigue, weight loss, pyrexia of unknown -origin, clubbing
  • Emboli
  • AF
  • Mid diastolic murmur

Echo show pedunculate heterogenous mass in fossa ovalis region

142
Q

What are the features of an atrial septal defect?

A

Ejection systolic murmur
Fixed splitting of S2

Mostly in ostium secundum - RBBB and right axis deviation

If in ostium primum - RBBB and left axis deviation, prolonged PR

143
Q

What is brugada syndrome?

A

Autosomal dominant condition
More common in asians
Cause sudden cardiac death

144
Q

What ECG changes are seen in brugada syndrome?

A

Coved ST elevation followed by negative t wave

Partial RBBB

More obviously seen when given flecainade

145
Q

How do you managed brugada syndrome?

A

Implantable ICD

146
Q

What is Burgers disease?

A

Small and medium vessel vasculitis associated with smoking

  • Extremity ischaemia - claudication and ulcers
  • Superficial thrombophlebitis
  • Raynaud’s
147
Q

What echo findings are associated with hypertrophic cardiomyopathy?

A

Mitral regurg
Systolic anterior motion of anterior mitral valve
Asymmetrical septal hypertrophy

148
Q

What commonly causes dilated cardiomyopathy?

A

Alcohol
Coxackie B
Wet beri beri
Doxorubicin

149
Q

What causes restrictive cardiomyopathy?

A

Amyloidosis
Post-radiotherapy
Loefflers endocarditis

150
Q

What are the types of acquired cardiomyopathy?

A

Peripartum

Takotsubo

151
Q

What is permpartum cardiomyopathy?

A

Develop between last month of pregnancy and 5 months post partum

More common in older women, greater parity or multiple gestation

152
Q

What is takotsubo’s cardiomyopathy?

A

Stress induced
Transient apical ballooning of myocardium
Supportive treatment

Broken heart

153
Q

What is coarctation of the aorta?

A

Narrowing of the descending aorta

More common in males

154
Q

What are the features of co-arctation of the aorta?

A

Infancy - heart failure
Adult - hypertension

Radiofemoral delay
Midsystolic murmur with apical click
Notching of inferior border of ribs

155
Q

What is coarctation of the aorta associated with?

A

Turners syndrome
Bicuspid aortic valve
Berry aneurysm
Neurofibromatosis

156
Q

What is DVLA guidance in hypertension?

A

Can continue

If group 2 - disqualified if consistently above 180/100

157
Q

What is DVLA guidance post angioplasty?

A

1 week off driving

158
Q

What is DVLA guidance post CABG and ACS?

A

CABG - 4 weeks off

ACS - 4 weeks off. 1 week if treated successfully by angioplasty

159
Q

What is DVLA guidance in angina?

A

Must stop if symptoms at rest

160
Q

What is DVLA guidance for pacemakers?

A

Insertion - 1 week off

If for sustained ventricular arrhythmia - 6 months off
If prophylactic - 1 month off

Can’t drive group 2 vehicles

161
Q

What is the driving guidance for successful catheter ablation?

A

2 days off driving

162
Q

What is the driving guidance for berry aneurysms?

A

Notify DVLA
License renewal reviewed annually
Diameter >6.5cm disqualify

163
Q

What is the driving guidance post heart transplant?

A

6 weeks off

Don’t need to inform DVLA

164
Q

What is eisenmengers syndrome?

A

Left to right shunt become right to left stunt because pressure build up in pulmonary system

Features:

  • Cyanosis
  • Clubbing
  • RV failure
  • Haemoptysis
  • Embolism

May need heart lung transplant

165
Q

What are the features of hypertrophic cardiomyopathy?

A

Often asymptomatic

  • Exertional dyspnoea
  • Angina
  • Syncope - follow exercise
  • Sudden death
  • Jerky pulse
  • Ejection systolic murmur - increase with valsalva, -decrease with squatting
166
Q

What ECG findings are associated with hypertrophic cardiomyopathy?

A

LV hypertrophy
Non specific ST and t wave abnormalities
Deep q waves
AF

167
Q

What is long qt syndrome associated with?

A

Sudden death
Exertional dyspnoea
Syncope

168
Q

How is long QT managed?

A

Avoid drugs that prolong QT

Beta blockers

ICD in high risk cases

169
Q

What is the diagnostic criteria for postural hypotension?

What are some causes?

A

> 20mm/Hg drop in systolic BP after 3 minutes of standing

  • hypovolaemia (dehydration)
  • autonomic dysfunction (diabetes, Parkinsons)
  • drugs (diuretics, alpha blockers, anti-HTN, sedatives)
  • alcohol
170
Q

How is orthostatic hypotension managed?

A

Stop precipitating drugs

Fludrocortisone and midodrine

171
Q

What is pulsus paradoxus and what causes it?

A

BP drop with inspiration

Asthma and Cardiac Tamponade

172
Q

What causes a slow rising pulse?

A

Aortic stenosis

173
Q

What causes a collapsing pulse?

A

Aortic regurgitation
PDA
Hyperkinetic states

174
Q

What is pulsus alterans and what causes it?

A

Regular alternation of force of pulse

Severe LV failure

175
Q

What causes a bisferens pulse?

A

Mixed aortic valve disease

HOCM* - can be associated

176
Q

What causes a jerky pulse?

A

HOCM

177
Q

What is rheumatic fever?

A

Immunological reaction to a recent step pyogenes infection (2-6 weeks prior)

178
Q

How is rheumatic fever diagnosed?

A

Evidence of strep pyogenes infection
+ 2 major or
+ 1 major and 1 minor

179
Q

What are the major criteria for rheumatic fever?

A 
Erythema marginatum
Sydenham's chorea
Polyarthritis
Carditis and valvulitis
Subcutaneous nodules
180
Q

What are the minor criteria for rheumatic fever?

A

Raised ESR
Pyrexia
Arthralgia
Prolonged PR

181
Q

How is rheumatic fever managed?

A

NSAIDs
PenV oral

treat complications

182
Q

What is takayasu’s arteritis?

A

Large vessel vasculitis occluding aorta leading to missing limb pulse

More common in women and asians

183
Q

What are the features of takayasu’s arteritis?

A 
Malaise, headache
Unequal pulses in limbs
Carotid bruit
Intermitted claudication
Aortic regurgitation

Associated with renal artery stenosis

184
Q

How is takayasu’s arteritis managed?

A

Steroids

185
Q

What is HF-REF?

A

AKA systolic HF
There is an INABILITY TO PUMP out blood so the ventricle DILATES to compensate. This can lead to the mitral valve being pulled open and then blood backing up to the atria

186
Q

What is HF-PEF?

A

AKA diastolic HF
There is an INABILITY TO RELAX/FILL so the ventricle HYPERTROPHYS to compensate. The deeper layers of muscle are not perfused so can become fibrotic

187
Q

When does right sided heart failure occur?

A

Rarely alone

  • Pulmonary HTN (Left sided HF or COPD)
  • right sided valve disease
  • pericardial pathology
188
Q

When else may BNP be raised? How should the result be interpreted in HF diagnosis?

A

Diabetes
CKD
COPD
Liver cirrhosis

If it is negative it’s likely not HF however if +ve do next step of investigations as not diagnostic

189
Q

How is HF-PEF managed?

A

Furosemide for symptoms

Refer to specialists

190
Q

A patient is on an ACE-I for HTN, when would you consider switching this and to what?

A

Intolerable cough = Angiotensin 2 antagonist

K>5.5 or Creatinine >30% baselines = CCB

191
Q

What defines malignant HTN and how would they present?

A

s>180 or d>120 + papilledema

  • retinal bleeding
  • RICP = headache
  • epistaxis
  • chest pain
  • haematuria
192
Q

How is malignant hypertension managed?

A

Labetalol and GTN infusion

193
Q

What are the causes of HTN?

A 
90% Primary/idiopathic
10% secondary 
- renal disease
- endocrine disease (pheochromocytoma, Cushing's, hyperaldosteronism
- pregnancy 
- COCP, steroids, NSAIDs, SSRI
194
Q

Although HTN is often asymptomatic, how might it present?

A

Palpitations
Angina
Headache
Blurred vision

195
Q

What are the stages of hypertensive retinopathy?

A
  1. arteriolar narrowing (silver wiring)
  2. arteriovenous nipping
  3. blot/flame haemorrhage, cotton wool spots
  4. papilledema
196
Q

What are some complications of HTN?

A 
HF
Stroke 
MI
Retinopathy 
CKD
197
Q

What is the grading of murmurs?

A

1: very faint
2: soft
3: easily heard
4: can hear thrill
5: audible with stethoscope partly off chest
6: audible with stethoscope fully of chest

198
Q

What is responsible for the 3rd and 4th heart sounds?

A

3rd: rush of blood into the ventricle
4th: atrial contraction of blood in to a stiff ventricle

199
Q

What defines typical vs atypical angina?

A

Typical: all 3
Atypical: 2/3

  • Constricting central chest discomfort
  • Precipitated by strenuous activity
  • Relieved in 10 minutes or after 2 GTN sprays
200
Q

What are the causes of angina?

A 
Atheroma (coronary artery disease)
Aortic stenosis
Coronary vasospasm (cocaine)
Vasculitis (Kawasaki) 
LV hypertrophy 
Tachyarrhythmias
Anaemia
201
Q

What advice regarding GTN and calling an ambulance should you give to angina patients?

A

take 2 sprays 5 minutes apart and if not relived after the second one (i.e. at 10 minutes) then call an ambulance

202
Q

What is the classification of angina?

A
  1. precipitated by strenuous activity
  2. precipitated by daily activities done fast paced
  3. precipitated by normal daily activities i.e. 1 flight of stairs
  4. rest pain
203
Q

What investigations are done at rapid access chest pain clinic? What results would you see?

A

ECG: pathalogical Q, ST and T wave changes, LBBB
Echo: valve pathology, motion abnormalities, LV dysfunction
Bloods: anaemia exacerbates

204
Q

What is the step wise approach to diagnosing angina?

A
  1. for people at low risk/ have no history of CAD
    - CT coronary angio
  2. functional testing - if obstruction seen on CT angio or if established CAD
    - dobutamine stress echo
    - SPECT
    - stress contrast MRI
  3. if positive functional tests, unresponsive to medical therapy, high risk of ACS or angina at low activity level
    - CABG or PCI
205
Q

What is Dressler’s syndrome?

A

Fever + pleuritic chest pain + raised ESR + pleural effusion
Occurs around a month after an MI

206
Q

What is the driving advice post STEMI?

A

not for 4 weeks

207
Q

What features define myocardial ischaemia?

A

Elevated troponin + one of:

  • Suggestive symptoms
  • Pathological Q waves
  • ST changes or new LBBB
  • Echo evidence of motion abnormality
  • Angiography evidence of occlusion
208
Q

What can causes myocardial ischaemia?

A 
Atherosclerosis
Vasculitis 
Coronary vasospasm
coronary dissection 
oxygen demand/delivery missmatch
- anaemia
- tachyarrhythmia
- hyperthyroid
- severe sepsis
209
Q

What are some differentials for ST elevation?

A

Pericarditis
Coronary vasospasm
Ventricular aneurysm

210
Q

What are some differentials for ST depression?

A

Electrolyte abnormalities
Digoxin effect
BBB

211
Q

What are some differentials for a raised troponin?

A 
HF
Tachyarrhythmia 
Myocarditis 
PE
and lots lots more
212
Q

How is NSTEMI/UA managed? What is this determined by?

A

Do a GRACE risk score and depending on outcome:

  • just aspirin
  • dual antiplatelet + fondaparinux
  • coronary angiography + UFH + dual antiplatelet (aspirin + prasugrel or clopidogrel if on anticoag)
213
Q

What factors contribute towards calculating a GRACE score?

A 
BP
HR
ECG changes
cardiac biomarkers 
Arrest 
Renal function
214
Q

When do you do PCI and when do you use fibrinolysis in ACS?

A

PCI

  • presenting within 12 hours and can get to centre within 120 minutes
  • presents >12 hours of symptom onset but has continuing ischaemic changes
  • ECG does not show resolution of symptoms 90 minutes after fibrinolysis

Fibrinolysis
- PCI not available within 120 minutes

215
Q

What drugs are given to a patient undergoing PCI?

A

Aspirin
Prasugrel (or clopidogrel if on antiplatelet)
UFH
Bailout GPI

216
Q

What drugs are given to a patient alongside doing fibrinolysis?

A 
Aspirin
Ticagrelor (or clopidogrel if ++ bleeding risk)
Antithrombin drug (UFH, fondaparinux etc.)
217
Q

What reciprocal changes would you expect in an a) anterolateral or lateral STEMI and b) inferior STEMI?

A

a) 2, 3, AVF

b) 1, AVL

218
Q

What ECG changes are seen in a posterior STEMI?

A

ST depression in V1-3
Dominant R wave in V1 (tall, broad and R/S ration >1)
ST elevation in leads V7-V9

219
Q

What artery occlusion is responsible for

a) inferior MI
b) lateral MI
c) anteroseptal MI?

A

a) RCA
b) Left circumflex
c) LAD

Finals (16 decks)

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