Cardiology Flashcards

1
Q

Pathology of AF

A

Left atrium loses its refractoriness before end of atrial systole
Gives recurrent uncoordinated contraction 300bpm
atrial contraction is responsible for around 25% CO thus it often triggers HF.

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2
Q

Causes of AF

A
Common
 IHD
 Rheumatic heart disease
 Thyrotoxicosis
 Hypertension
Other
 Alcohol
 Pneumonia
 PE
 Post-op
 Hypokalaemia
 RA
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3
Q

Symptoms AF

A
Symptoms
 Asympto
 Chest pain
 Palpitations
 Dyspnoea
 Faintnes
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4
Q

Signs AF

A

Signs

 Irregularly irregular pulse
 Pulse deficit: difference between pulse and HS
 Fast AF → loss of diastolic filling → no palpable pulse
 Signs of LVF

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5
Q

Investigations AF

A
  • ECG
     FBC, U+E, TFTs, Trop
     Consider TTE: structural abnormalities
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6
Q

Management acute AF

A

haemodynamically unstable –
1st line – emergency cardioversion
2nd line – IV amiodarone

control ventricular rate:
1st line – diltiazem/verapamil/metoprolol
2nd line – digoxin or amiodarone

start LMWH

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7
Q

Cardioversion in AF

A

only done in acute causes <48 hours

electrical or pharmacological
Pharm:
1st line – flecainide if no structural heart disease
2nd line – amiodarone IV

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8
Q

Flecainide MOA

A

sodium channel blocker

slows upstroke of cardiac action potential

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9
Q

Paroxysmal AF

A

a self limiting flare up of AF lasting less than 7 days with recurrence tendency

use CHADSVASC to decide to anticoagulate

Treatment with pill in pocket
(flecainide) to manage flare up

Prevention

  • B blocker
  • Sotalol
  • amiodarone
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10
Q

What is persistent AF

A

AF lasting > 7 days

may recur even after cardioversion

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11
Q

How to treat persistent AF

A

Try rhythm control if:

  • symptomatic
  • age< 65
  • first incidence
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12
Q

What is rhythm control treatment AF

A

Rhythm Control (cardioversion) need to follow these steps as it is a risky treatment
 TTE first: look for structural abnormalities
 Anticoagulate ̄c warfarin for ≥3wks
 or use TOE to exclude intracardiac thrombus.
 Pre-Rx ≥4wks ̄c sotalol or amiodarone if ↑ risk of failure
 Electrical or pharmacological cardioversion eg flecainide (this is the treatment step)
 ≥ 4 wks anticoagulation afterwards (target INR 2.5)

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13
Q

AF maintenance antiarrhythmic

A

Not needed if successfully treated precipitant
1st line — B blocker
2nd line – amiodarone

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14
Q

Final options for AF treatment

A

radiofrequency ablation of AV node
Maze procedure create scar tissue
Pacing

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15
Q

Rate control for AF

A

This is used when can’t do rhythm control
Target HR <90

1st line – B blocker or rate limiting CCB (not together)
2nd line – add digoxin
3rd line – Consider amiodarone

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16
Q

When to use rate control in AF

A

failed cardioversion
patient doesn’t want cardioversion
AF>1 year/ valve disease/ poor LV function

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17
Q

Management of atrial flutter

A

manage as for AF
drugs may not work

amiodarone to restore sinus
amiodarone to maintain sinus

cavotricuspid isthmus ablation right atrium is treatment of choice.

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18
Q

CHA2DS2VAS score

A

determines necessity of anticoagulation in AF

CCF
HTN
AGE >75 (2 points)
Diabetes
Stroke or TIA (2 points)
Vascular disease
Age 65-74 
Sex female 

Score
1- aspirin 300mg
2+ - warfarin

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19
Q

Acute coronary syndrome definition

A

unstable angina + evolving MI

ST elevation or new onset LBB
NSTEMI

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20
Q

Pathophysiology of ACS

A

plaque rupture
thrombosis
inflammation

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21
Q

Symptoms ACS

A
acute central chest pain < 20mins
radiates to left arm/jaw
nausea
sweating
dyspnoea
palpitations
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22
Q

Signs of ACS

A
anxiety
pallor sweating
pulse up then down
BP up then down
4th heart sound
signs of LVF 
- basal crepitations, raised JVP, 3rd HS
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23
Q

DDX of ACS

A
angina
peri/endo/myo carditits
dissection
PE, pneumothorax, pneumonia
costochondritis
GORD
anxiety
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24
Q

Investigations ACS

A
ECG
Bloods
- troponin
- FBC
-U&amp;E
- glucose
-lipids
-INR
CXR
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25
STEMI ECG
``` STEMI Sequence  Normal  ST elevation + hyperacute (tall) T waves  Q waves: full-thickness infarct  Normalisation of ST segments  T wave inversion  (New onset LBBB also = STEMI) ```
26
NSTEMI ECG
ST depression | T wave inversion
27
Subendocardial infarct ECG
No Q waves
28
Inferior MI ECG
2 3 avf vessel RCA
29
anterolateral MI ECG
1 avl V4-V6 vessel LCx
30
Anteroseptal MI ECG
V2-V4 vessel LAD
31
Anterior MI ECG
V2-V6 vessel LMCA
32
Posterior MI ECG
V1-V3 reciprocal changes vessel RCA
33
ACS blood results
Troponin T and I look at 3 and 12 hours peak 24 hours returns to baseline 5-14 days
34
CXR ACS
cardiomegaly pulmonary oedema widened mediastinum - aortic rupture
35
ACS diagnosis
STEMI/LBB - typical symptoms + ST elevation / LBB NSTEMI - typical symptoms + no ST elevation + +ve troponin UA - typical symptoms + no ST elevation + -ve troponin
36
STEMI treatment brief
PCI or thrombolysis
37
NSTEMI/UA treatment brief
medical + elective angioplasty +- PCI/CABG
38
MI complications
Death Passing PRAED st. Death- VF, LVF, CVA Pump failure Pericarditis - mild fever pericardial friction rub relieved by sitting forward, ECG saddle shaped ST elevation, give ibuprofen Rupture - myomalacia cordis, cardiac tamponade giving beck's triad (drop BP, rise JVP, muffled heart sounds) and pulsus paradoxus. Papillary muscle = Mitral regurg. septum = heart failure Arrhythmias Aneurysm- ventricular Embolism from LV mural thrombus Dressler's syndrome - autoantibodies against myocyte sarcolemma read through notes following this flashcard more info
39
Pulsus paradoxus
drop in systolic BP >10mmHg on inspiration
40
STEMI management
``` MONAC Morphine- 5-10mg IV Metoclopramide - 10mg IV Oxygen - 2-4L sats 94-98% Nitroglycerin - 2 puffs Aspirin 300mg PO then 75mg/day Clopidogrel - 300mg po then 75mg/day ``` 12 lead ECG LMWH eg enoxaparin IV then subcut Admit to CCU Primary PCI or thrombolysis
41
Choosing PCI or thrombolysis
PCI if <12 hours Thrombolysis if >24 hours from pain onset If not suitable for either then give fondaparinux
42
What does PCI involve
angioplasty and stenting + GP IIA/IIIA antagonist eg clopidogrel, tirofiban - give this if patient is delayed PCI, diabetes, complex
43
Complications of PCI
bleeding emboli arrhythmia
44
ECG criteria for thrombolysis
ST elevation >1mm in 2+ limb leads or >2mm in 2+ chest leads New LBBB Posterior MI - DEEP ST depression in V1-V3 and tall R waves
45
Contraindications for thrombolysis
AGAINST ``` Aortic dissection GI bleeding Allergic reaction previously Iatrogenic- recent surgery Neuro- cerebral neoplasm Severe HTN Trauma - including CPR ```
46
Thrombolysis drugs
Alteplase (tissue plasminogen activator ) streptokinase tenecteplase
47
Complications thrombolysis
bleeding stroke arrhythmia allergic reaction
48
Continuing therapy post MI
ACEi- start within 24 hours B blocker Aspirin (+- clopidogrel) statin and cardiac rehabilitation programme lifestyle advice
49
lifestyle advice post MI
``` stop smoking diet- oily fish, decrease sat fats exercise 30min/day work== return in 2 months sex == avoid 1 month driving== avoid 1 month ```
50
NSTEMI and UA management
MONAC fondaparinux 12 lead ECG GRACE score High risk - persistent recurrent ischaemia, ST depression, DM, positive troponin Low risk- No pain , flat or inverted T waves, normal ECG, negative troponin
51
GRACE score
used to assess ACS risk
52
Managing high risk GRACE UA NSTEMI
GP2a/3a antagonist- tirofiban angiography +- PCI within 96 hours clopidogrel 75mg/day for one year
53
Managing low risk GRACE UA NSTEMI
may discharge after 12 hours if troponin negative follow up outpatient tests - angiography - perfusion scan - stress echo
54
Angina pectoris pathophysiology
atherosclerosis leading to ischaemia
55
Causes of angina
``` mostly atheroma anaemia aortic stenosis tachyarrhythmias arteritits ```
56
Symptoms angina pectoris
central chest tightness brought on by exertion and relieved by rest may radiate to arms/jaw precipitants - emotion, cold weather, heavy meals
57
Classification of Angina
Stable - induced by effort Unstable - occurs at rest, minimal exertion Decubitus - induced by lying down Variant - at rest due to coronary spasm, gives ST elevation during attack, treat with CCB and long acting nitrate Syndrome X - angina pain and ST elevation on exercise test no evidence of coronary atherosclerosis
58
DDX angina
Aortic stenosis Aortic aneurysm GORD chostrochondritis
59
Investigations angina
``` Angiography (gold standard) Bloods - FBC UE lipids glucose ESR TFTs ECG - usually normal Exercise ECG Stress echo Perfusion scan CT coronary calcium score ```
60
Management of angina pectoris overview
Lifestyle Medical Interventional Surgical
61
Medical management angina
secondary prevention - aspirin - ACEi - Statin - Antihypertensive ``` Anti anginals - GTN spray/sublingual + B blocker + CCB + Both (Amlodipine) ``` + ivabradine +nicorandil
62
Interventional management of angina pectoris
What -PCI When - poor response to medical treatment - not suitable for CABG Complications - restenosis - MI - Death clopidogrel reduces risk of restenosis best to use drug eluting stent as well
63
Surgical management of Angina
What - CABG When - LMCA disease - Triple vessel disease - Refractory angina - Unsuccessful PCI Complications - stroke - MI - Pericardial tamponade - Post perfusion syndrome - Post op AF - Graft stenosis
64
Heart failure definition
CO is inadequate for the body's requirements despite adequate filling pressures
65
Pathophysiology of Heart failure
``` Initial reduction in CO== compensation starling effect dilates heart to enhance contractility remodelling == hypertrophy RAAS activation ANP/BNP release Sympathetic activation ``` Progressive decline in CO == decompensation progressive dilation gives impaired contractility and valve regurgitation hypertrophy leads to relative myocardial ischaemia RAAS activation leads to Na+ retention and fluid retention == increased venous pressure and oedema sympathetic excess - increased afterload and decreased CO
66
Causes of low output cardiac failure
Low output cardiac failure is when CO drops and it can't increase with exertion ``` 1. Pump failure: Systolic failure → impaired contraction  Ischaemia/MI (commonest cause)  Dilated cardiomyopathy  Hypertension  Myocarditis ``` Diastolic failure → impaired filling  Pericardial effusion / tamponade / constriction  Cardiomyopathy: restrictive, hypertrophic Arrhythmias  Bradycardia, heart block  Tachycardias  Anti-arrhythmics (e.g. beta-blocker, verapamil) ``` 2. Excessive pre-load  AR,MR  Fluid overload t 3. Excessive afterload  AS  HTN  HOCM hypertrophic cardiomyopathy ```
67
Causes of high output cardiac failure
This is when body has increased needs which the heart can't meet, initially gives RVF then LVF. Anaemia, Arteriovenous malformation Thyrotoxicosis, Thiamine deficiency (beri Beri) Pregnancy, Pagets
68
What are the causes, symptoms and signs of RVF
Causes: - LVF - Cor pulmonale - Tricuspid and pulmonary valve disease Symptoms: - Anorexia - Nausea ``` Signs:  ↑JVP + jugular venous distension  Tender smooth hepatomegaly (may be pulsatile)  Pitting oedema  Ascites ```
69
LVF causes symptoms and signs
``` Causes  1st: IHD  2nd: idiopathic dilated cardiomyopathy  3rd: Systemic HTN  4th: Mitral and aortic valve disease  Specific cardiomyopathies ``` Symptoms  Fatigue  Exertional dyspnoea  Orthopnoea + PND paroxysmal nocturnal dyspnoea  Nocturnal cough (± pink, frothy sputum)  Wt. loss and muscle wasting ``` Signs  Cold peripheries ± cyanosis  Often in AF  Cardiomegaly ̄c displaced apex  S3 + tachycardia = gallop rhythm  Wheeze (cardiac asthma)  Bibasal creps ```
70
Chronic HF FRAMINGHAM Criteria
For CCF diagnosis need 2 major or 1 major + 2 minor Major: - Paroxysmal nocturnal dyspnoea - Neck vein distension - Cardiomegaly - Acute pulmonary oedema - Increase CVP
71
CCF Investigations
Bloods- FBC UE BNP TFTs glucose lipids CXR - ABCDE (Alveolar shadowing bats wings, B kerley lines, Cardiomegaly, Dilated upper veins, Effusions) ECG- Ischaemia, hypertrophy, AF Echocardiogram - Hypertrophy, valve lesions, Intracardiac shunts, Reduced ejection fraction, hypokinesia
72
BNP actions and use as a marker
Actions:  ↑ GFR and ↓ renal Na reabsorption  ↓ preload by relaxing smooth muscle Marker:  ↑ BNP (>100) better than any other variable and clinical judgement in diagnosing heart failure  BNP correlates ̄c LV dysfunction  i.e. ↑ most in decompensated heart failure  ↑ BNP = ↑ mortality  BNP <100 excludes heart failure (96% NPV)  BNP also ↑ in RHF: cor pulmonale, PE
73
New York Heart Association Classification
1. No limitation of activity 2. Comfortable @ rest, dyspnoea on ordinary activity 3. Marked limitation of ordinary activity 4. Dyspnoea @ rest, all activity → discomfort
74
CCF specific management
1st line: ACEi/ARB + B Blocker + Loop Diuretic with B blockers start low and go slow 2nd line: K+ saving diuretic - spironolactone (watch for hyperkalaemia especially if on ACEi as well) ACEi + ARB Vasodilators (hydralazine + ISDN) 3rd line: Digoxin ICD
75
Things to monitor in chronic CCF
BP may be very low Renal function Plasma K if on spironolactone and ACEi Daily weight
76
Management severe pulmonary oedema
1. Sit patient up 2. Oxygen 15L non rebreath mask target 94-98% 3. IV access and monitor ECG (bloods and treat any arrhythmias 4. Diamorphine 2.5-5mg IV (pain and is pulmonary venodilator) + metoclopramide 10mg IV 5. Furosemide 40-80mg IV 6. GTN 2 puffs or 2 buccal tablets (unless SBP<90) 7. If SBP>100 start nitrate infusion 8. if worsening consider CPAP dialysis If SBP drops below 100 treat as cardiogenic shock and give inotropes
77
Causes severe pulmonary oedema cardiac and non cardiac
Cardiogenic  MI  Arrhythmia  Fluid overload: renal, iatrogenic Non-cardiogenic  ARDS: sepsis, post-op, trauma  Upper airway obstruction  Neurogenic: head injury
78
Pulmonary oedema symptoms
Dyspnoea Orthopnoea pink frothy sputum
79
Pulmonary oedema signs
``` Distressed, sweaty, cyanosed Tachycardia Tachypnoea Raised JVP S3 gallop rhythm Bibasal crepitations Pleural effusions Wheeze ```
80
Pulmonary oedema DDx
Asthma COPD Pneumonia PE
81
Cardiogenic shock definition
decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. the failure of CO is due to pump failure
82
Management cardiogenic shock
1. Oxygen 15L nonrebreath mask 94-98% 2. IV access and monitor ECG 3. Diamorphine 2.5-5mg IV + metoclopramide 4. Correct any arrhythmias, electrolyte disturbances, acid-base abnormalities 5. CXR, Echo, CT thorax 6. Monitor CVP, BP, ABG, ECG, Urine 7. Consider need for inotropes dobutamine 8. Treat underlying cause
83
Causes of cardiogenic shock
MI HEART ```  MI  Hyperkalaemia (inc. electrolytes)  Endocarditis (valve destruction)  Aortic Dissection  Rhythm disturbance  Tamponade ``` + obstructive causes - Tension pneumothorax - Massive PE
84
Presentation of cardiogenic shock
Unwell, pale, sweaty, cyanosed, distressed cold clammy peripheries, ↑RR ± ↑HR Pulmonary oedema
85
Cardiac tamponade causes
```  Trauma  Lung/breast Ca  Pericarditis  MI  Bacteria (e.g. TB) ```
86
Cardiac tamponade signs
 Beck’s triad: ↓BP, ↑JVP, muffled heart sounds  Kussmaul’s sign: ↑JVP on inspiration  Pulsus paradoxus (pulse fades on inspiration)
87
Cardiac tamponade investigations
Echo - diagnostic | CXR - globular heart
88
Cardiac tamponade Management
ABCDE | Pericardiocentesis using echo guidance is best
89
Hypertension definitions stages
```  Stage 1: Clinic BP > 140/90  Stage 2: Clinic BP > 160/100  Severe: Clinic BP > 180/110  Malignant: BP > 180/110 + papilloedema and/or retinal haemorrhage  Isolated SHT: SBP ≥140, DBP <90 ```
90
Causes of Hypertension
PREDICTION ``` Primary/Essential 95% Renal - RAS, glomerulonephritis, PKD Endocrine - Hyperthyroid, cushing's, phaeochromocytoma, acromegaly, conn's Drugs- cocaine, cocp, NSAIDS ICP raised Coarctation of aorta Toxaemia of pregnancy Increased viscocity Overload with fluid Neurogenic ```
91
Clues for hypertension cause
``` Increased HR thyrotoxicosis Radio-femoral delay = Coarctation of aorta Renal bruits = Renal artery stenosis Palpable kidneys = PKD Paroxysmal symptoms = phaeochromocytoma ```
92
Hypertension end organ damage
CANER Cardiac  IHD  LVH → CCF  AR,MR Aortic  Aneurysm  Dissection Neuro  CVA: ischaemic, haemorrhagic  Encephalopathy (malignant HTN) Eyes - hypertensive retinopathy Keith-Wagener Classification: 1. Tortuosity and silver wiring 2. AV nipping 3. Flame haemorrhages and cotton wool spots 4. Papilloedema grades 3 and 4 signify malignant hypertension Renal - proteinuria - CKD
93
Hypertension investigations
24 HR ABPM Urine - haematuria Albumin:creatinine ratio Bloods - FBC, UE eGFR glucose fasting lipids 12 lead ECG - LVH, old infarct Calculate 10 year CV risk Q score important to do ABPM first before starting treatment so you can confirm diagnosis
94
What are the indications for pharmacological management in hypertension
<80yrs, stage 1 HTN (>140/90) and one of:  Target organ damage (e.g. LVH, retinopathy)  10yr CV risk ≥20%  Established CVD  DM  Renal disease  Anyone with stage 2 HTN (>160/100)  Severe / malignant HTN (specialist referral)  Consider specialist opinion if <40yrs with stage 1 HTN and no end organ damage.
95
Hypertension BP targets
 Under 80yrs: <140/90 (<130/80 in DM) |  Over 80yrs: <150/90
96
Antihypertensive treatment
1. <55 = A > 55 or black = C 2. A+C 3. A+C+D 4. A+C+D + consider further diuretic eg spironolactone + consider a blocker or B blocker + seek expert opinion A: ACEi or ARB  e.g. lisinopril 10mg OD (↑ to 30-40mg)  e.g. candesartan 8mg OD (max 32mg OD) C: CCB: e.g. nifedipine MR30-60mg OD D: Thiazide-like diuretic: e.g. chlortalidone 25-50mg OD In step 2, use ARB over ACEi in blacks. Avoid thiazides + β-B if possible (↑ risk of DM). Only consider β-B if young and ACEi/ARB not tolerated.
97
How to manage malignant HTN
 Controlled ↓ in BP over days to avoid stroke  Atenolol or long-acting CCB PO  Encephalopathy/CCF: fruse + nitroprusside / labetalol IV  Aim to ↓ BP to 110 diastolic over ~4h  Nitroprusside requires intra-arterial BP monitoring
98
Aortic stenosis causes
 Senile calcification (60yrs +): commonest  Congenital: Bicuspid valve (40-60yrs), William’s syn.  Rheumatic fever
99
Aortic stenosis symptoms
```  Triad: angina, dyspnoea, syncope (esp. ̄c exercise)  LVF: PND, orthopnoea, frothy sputum  Arrhythmias  Systemic emboli if endocarditis  Sudden death ```
100
Aortic stenosis signs
 Slow rising pulse ̄c narrow PP  Aortic thrill  Apex: Forceful, non-displaced (pressure overload) Heart Sounds  Quiet A2  Early syst. ejection click if pliable (young) valve  S4 (forceful A contraction vs. hypertrophied V) ``` Murmur  ESM  Right 2nd ICS  Sitting forward in end-expiration  Radiates to carotids ```
101
Aortic stenosis DDX
```  Coronary artery disease  MR  Aortic sclerosis  Valve thickening: no pressure gradient  Turbulence → murmur  ESM ̄c no radiation and normal pulse ``` HOCM  ESM murmur which ↑ in intensity ̄c valsalva (AS↓)
102
Aortic stenosis investigations
Bloods: ECG:  LVH  LV strain: tall R, ST depression, T inversion in V4-V6  LBBB or complete AV block (septal calcification)  May need pacing ``` CXR  Calcified AV (esp. on lateral films)  LVH  Evidence of failure  Post-stenotic aortic dilatation ``` Echo + Doppler: diagnostic  Thickened, calcified, immobile valve cusps Cardiac Catheterisation + Angiography  Can assess valve gradient and LV function  Assess coronaries in all pts. planned for surgery Exercise Stress Test  Contraindicated if symptomatic AS  May be useful to assess ex capacity in asympto pts.
103
Medical management aortic stenosis
 Optimise RFs: statins, anti-hypertensives, DM  Monitor: regular f/up ̄c echo  Angina: β-B  Heart failure: ACEi and diuretics
104
Surgical management aortic stenosis
``` Poor prog. if symptomatic  Angina/syncope: 2-3yrs  LVF: 1-2yrs Indications for valve replacement  Severe symptomatic AS  Severe asymptomatic AS ̄c ↓ EF (<50%)  Severe AS undergoing CABG or other valve op Valve types  Mechanical valves last longer but need anticoagulation: young pts.  Bioprosthetic don’t require anticoagulation but fail sooner (10-15yrs) ```
105
Aortic regurgitation causes
Acute: Infective endocarditis Type A aortic dissection ``` Chronic: Congenital - bicuspid aortic valve Rheumatic heart disease Connective tissue disease: Marfan's , Ehler's danlos Autoimmune: ankylosing spondylitis RA ```
106
Aortic regurgitation symptoms
 LVF: Exertional dyspnoea, PND, orthopnoea  Arrhythmias (esp. AF) → palpitations  Forceful heart beats  Angina
107
Aortic regurgitation signs
 Collapsing pulse (Corrigan’s pulse)  Wide PP  Apex: displaced (volume overload) Heart Sounds  Soft / absent S2  ± S3 ``` Murmur  Early DM decrescendo  UR Sternal Edge + 3rd left IC parasternal  Sitting forward in end-expiration  ± ejection systolic flow murmur  ± Austin-Flint murmur ``` Underlying cause  High-arched palate  Spondyloarthropathy  Embolic phenomena
108
Investigations aortic regurgitation
Bloods: FBC, U+E, lipids, glucose ECG: LVH (R6+S1 > 35mm) CXR  Cardiomegaly  Dilated ascending aorta  Pulmonary oedema Echo  Aortic valve structure and morphology (e.g. bicuspid)  Evidence of infective endocarditis (e.g. vegetations) Cardiac Catheterisation  Coronary artery disease  Assess severity, LV function, root size
109
Management of aortic regurgitation
Medical basically just manage the risk factors HTN, DM etc and have regular follow up Surgical Aortic valve replacement reserved for severe cases with HF symptoms
110
Mitral Stenosis causes
Rheumatic fever Prosthetic valve Congenital
111
Mitral stenosis pathophysiology consequences
 Valve narrowing → ↑ left atrial pressure → loud S1 and atrial hypertrophy → AF  → pulmonary oedema and PHT → loud P2, PR  → RVH → left parasternal heave  →TR→largevwaves  → RHF → ↑JVP , oedema, ascites
112
Mitral stenosis symptoms
``` Dyspnoea Fatigue Chest pains AF == palpitations and emboli haemoptysis == rupture of bronchial veins due to dilated rleft atrium ```
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Mitral stenosis signs
Symptoms manifest when orifice <2cm2 (norm 4-6)  AF, low volume pulse  Malar flush (↓CO → backpressure + vasoconstriction) JVP may be raised late on  Prominent a waves: PTH  Large v waves: TR  Absent a waves: AF  Left parasternal heave (RVH secondary to PHT)  Apex: Tapping (palpable S1), non-displaced Heart sounds  Loud S1  Loud P2 (if PHT)  Early diastolic opening snap ``` Murmur  Rumbling MDM  Apex  Left lateral position in end expiration  Radiates to the axilla  ± Graham Steell murmur (EDM 2O to PR) ```
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What are heaves a sign of
Hypertrophy
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What are thrills a sign of
Palpable murmur
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Complications of Mitral stenosis
 Pulmonary HTN  Emboli: TIA, CVA, PVD, ischaemic colitis  Hoarseness: rec laryngeal N. palsy = Ortner’s Syn  Dysphagia (oesophageal compression)  Bronchial obstruction
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Mitral stenosis investigations
Bloods: FBC, U+E, LFTs, glucose, lipids ECG  AF  P mitrale (if in sinus)  RVH ̄c strain: ST depression and T wave inversion in V1-V2 CXR  LA enlargement  Pulmonary oedema: ABCDE  Mitral valve calcification Echo and doppler Severe MS (AHA 2006 Criteria)  Valve orifice <1cm2  Pressure gradient >10mmHg  Pulmonary artery systolic pressure >50mmHg Use TOE to look for left atrial thrombus if intervention considered. Cardiac Catheterisation  Assess coronary arteries
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Management of mitral stenosis
Medical monitor risk factors and treat them prophylaxis for rheumatic fever Treat AF Surgical  Indicated in mod–severe MS (asympto and symptomatic) ``` Percutaneous balloon valvuloplasty  Rx of choice  Suitability depends on valve characteristics  Pliable, minimally calcified  CI if left atrial mural thrombus ```  Surgical valvotomy / commissurotomy: valve repair  Valve replacement if repair not possible
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Mitral regurgitation causes
 Mitral valve prolapse  LV dilatation: AR, AS, HTN  Annular calcification → contraction (elderly)  Post-MI: papillary muscle dysfunction/rupture  Rheumatic fever  Connective tissue: Marfan’s, Ehlers-Danlos
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Mitral regurgitation symptoms
Dyspnoea fatigue AF == palpitations and emboli Pulmonary congestion == Hypertenison and oedema
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Mitral regurgitation signs
 AF  Left parasternal heave (LVH) Apex: displaced  Volume overload as ventricle has to pump forward SV and regurgitant volume  → eccentric hypertrophy Heart Sounds  Soft S1  S2 not heard separately from murmur  Loud P2 (if PTH) ``` Murmur  Blowing PanSystolicMurmur  Apex  Left lateral position in end expiration  Radiates to the axilla ```
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Mitral regurgitation investigations
Bloods: FBC, U+E, glucose, lipids ECG  AF  P mitrale (unless in AF)  LVH CXR  LA and LV hypertrophy  Mitral valve calcification  Pulmonary oedema Echo - Doppler echo to assess severity - TOE to assess severity and suitability of repair Cardiac Catheterisation  Confirm Dx  Assess CAD
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Management of mitral regurgitation
Medical Control risk factors Control AF Drugs to reduce afterload ``` Surgical  Valve replacement or repair Indications  Severe symptomatic MR  Severe asympto MR ̄c diastolic dysfunction: ↓EF ```
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Mitral valve prolapse (barlow syndrome)
Most common valve problem | Gives mitral regurgitation
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Barlow syndrome causes
```  Primary: myxomatous degeneration  Often young women  MI  Marfan’s, ED  Turner’s ```
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Barlow syndrome symptoms and signs
``` Symptoms  Usually asymptomatic  Autonomic dysfunction: Atypical chest pain, palpitations, anxiety, panic attack  MR: SOB, fatigue ``` Signs:  Mid-systolic click ± late-systolic murmur
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Tricuspid regurgitation causes
Functional RV dilation Rheumatic fever Infective endocarditis especially IVDU Carcinoid syndrome
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Tricuspid regurgitation symptoms
Fatigue hepatic pain on exertion Ascites Oedema
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Tricuspid regurgitation signs
 ↑JVP ̄c giant V waves  RV heave Murmur:  PanSystolicMurmur  LowerLeftSternalEdge in inspiration (Carvallo’s sign)  Pulsatile hepatomegaly  Jaundice
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Tricuspid stenosis causes
Rheumatic fever with comorbid mitral valve and aortic valve disease
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Tricuspid stenosis symptoms
Fatigue Ascites oedema
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Tricuspid stenosis signs
``` Increased JVP Opening snap Murmur: - End diastolic murmur - Lower left sternal edge in inspiration ```
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Pulmonary regurgitation causes
Any cause of pulmonary hypertension | If PR is secondary to Mitral stenosis = Graham Steel murmur
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Pulmonary regurgitation signs
Murmur Decrescendo early diastolic murmur heard at left upper sternal edge
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Pulmonary stenosis causes
``` Usually congenital Turner's syndrome Tetralogy of fallot rheumatic fever carcinoid syndrome ```
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Pulmonary stenosis symptoms
Dyspnoea fatigue ascites oedema
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Pulmonary stenosis signs
``` JVP changes RV heave Murmur - crescendo decrescendo systolic murmur - ULSE radiates to left shoulder ```
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Infective endocarditis definition
Cardiac valves develop vegetations composed of bacteria and platelet-fibrin thrombus
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infective endocarditis risk factors
``` Prosthetic valves Degenerating valvulopathy Congenital abnormality Rheumatic fever Post-op wounds IVDU== especially tricuspid valve Immunocompromised including DM ```
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Cause of infective endocarditis
Bacterial infection +ve S.aureus -ve Haemophilus Non-infective SLE
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Infective endocarditis clinical features
Sepsis - fever - rigors - Anaemia - Clubbing Embolic phenomena - Janeway lesions - abscesses in brain, heart, kidney, spleen Cardiac - New murmur MR most common - atrio-ventricular block - LV failure Immune complex deposition - Haematuria due to glomerulonephritis - Vasculitis - Roth spots - Splinter haemorrhages - Osler's nodes Roth spots are boat shaped retinal haemorrhages with pale centre
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How to diagnose infective endocarditis
Use Duke criteria Diagnose if 2 major, 1 Maj + 3 min , all 5 minor Major 1. +ve blood culture  Typical organism in 2 separate cultures, or  Persistently +ve cultures, e.g. 3, >12h apart 2. Endocardium involved  +ve echo (vegetation, abscess, valve dehiscence) or  New valvular regurgitation Minor 1. Predisposition: cardiac lesion, IVDU 2. Fever >38 3. Emboli: septic infarcts, splinters, Janeway lesions 4. Immune phenomenon: GN, Osler nodes, Roth spots, RF 5. +ve blood culture not meeting major criteria
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Investigations
``` Bloods  N.chromic, N.cytic anaemia  ↑ESR, ↑CRP  +ve IgG RF (immune phenomenon)  Cultures x 3, >12h apart  Serology for unusual organisms ``` Urine: Micro haematuria ECG: AV block Echo  TTE detects vegetations > 2mm  TOE is more sensitive (90-100% vs. 50-60%)
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Treatment infective endocarditis
Empiric = Acute sever -- flucloxacillin and gentamicin IV = Subacute -- Benzylpenicillin + gentamicin IV Then once bacteria is elucidated treatment is accordingly
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different antibiotics for different agents in infective endocarditis
 Streps: benpen + gent IV  Enterococci: amoxicillin + gent IV  Staphs: fluclox ± rifampicin IV  Fungi: flucytosine IV + fluconazole PO.  Amphotericin if flucytosine resistance or Aspergillus.
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Mortality for infective endocarditis
30% with staphs
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Rheumatic fever Cause
Group A beta haemolytic strep. pyogenes
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Epidemiology of rheumatic fever
5-15 years rare in west common in developing world Only 2% of population susceptible
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Pathophysiology of rheumatic fever
Antibody cross reactivity following strep pyogenes infection gives T2 hypersensitivity reaction due to molecular mimicry Abs attack Myosin protein in cell wall Cross react and creates damage Pathology gives Aschoff bodies and Anitschkow myocytes
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How to diagnose rheumatic fever
use the revised Jones criteria evidence of Group A strep infection + 2 major criteria or evidence of GAS infection + 1 major + 2 minor ``` Evidence of GAS infection  +ve throat culture  Rapid strep Ag test  ↑ ASOT or DNase B titre  Recent scarlet fever ``` ``` Major Criteria  Pancarditis  Arthritis  Subcutaneous nodules  Erythema marginatum  Sydenham’s chorea ``` ``` Minor criteria  Fever  ↑ESR or ↑CRP  Arthralgia (not if arthritis is major)  Prolonged PR interval (not if carditis is a major)  Prev rheumatic fever ```
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What are the symptoms of rheumatic fever
``` Pancarditis (60%)  Pericarditis: chest pain, friction rub  Myocarditis: sinus tachy, AV block, HF, ↑CK, T inversion  Endocarditis: murmurs  MR, AR, Carey Coombs’ (MDM) ``` Arthritis (75%)  Migratory polyarthritis of large joints (esp. knees) ``` Subcutaneous nodules (2-20%)  Small mobile, painless nodules on extensor surfaces (esp. elbows) ``` ``` Erythema marginatum (2-10%)  Red, raised edges ̄c central clearing.  Trunk, thighs and arms. ``` Sydenham’s Chorea (10%)  Occurs late  Grimacing, clumsy, hypotonia (stops in sleep)
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Investigations rheumatic fever
Bloods  Strep Ag test or ASOT  FBC, ESR/CRP ECG Echo
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Treatment of rheumatic fever
``` Bed rest until CRP normalises BENPEN IM 10 days Analgesia ASPIRIN add oral prednisolone if CCF of chorea symptoms give HALDOL or DIAZEPAM ```
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Prognosis of rheumatic fever
Attacks last around 3 months 60% with carditis will develop chronic rheumatic heart disease Mitral valve disease is very common complication Secondary prophylaxis helps prevent recurrence take peniciliin po for a while depending on initial severity
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Acute pericarditis causes
Causes  Viral: coxsackie, flu, EBV, HIV  Bacterial: pneumonia, rheumatic fever, TB, staphs  Fungi  MI, Dressler’s  Drugs: penicillin, isoniazid, procainamide, hydralazine  Other: uraemia, RA, SLE, sarcoid, radiotherapy
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acute pericarditis clinical features
Clinical Features ``` Central / retrosternal chest pain  Sharp  Pleuritic  Worse lying down  Relieved by sitting forward  Radiates to left shoulder ```  Pericardial friction rub.  Fever  Signs of effusion / tamponade
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acute pericarditis investigations
ECG - saddle shaped ST elevation - PR depression Bloods - FBC - troponin may be raised - cultures - virology
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Management of acute pericarditis
Analgesia ibuprofen Treat cause Consider steroids and immunosuppression
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Constrictive pericarditis cause
Heart becomes encased in rigid pericardium often unknown cause often follows acute pericarditis
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Clinical features of constrictive pericarditis
``` Clinical features  RHF ̄c ↑JVP (prominent x and y descents)  Kussmaul’s sign: ↑JVP ̄c inspiration  Quiet heart sounds  S3  Hepatosplenomegaly  Ascites, oedema ```
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Investigations of constrictive pericarditis
CXR - small heart and pericardial calcification Echo Cardiac catheterisation
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cause if 3rd heart sound
A third heart sound occurs early in diastole. In young people and athletes it is a normal phenomenon. In older individuals it indicates the presence of congestive heart failure. The third heart sound is caused by a sudden deceleration of blood flow into the left ventricle from the left atrium
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Cause of 4th heart sound
Forceful atria contraction in late diastole to force blood into ventricle which wont expand any further
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Management of constrictive pericarditis
surgical excision of the heart from it's restricting chamber
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Pericardial effusion cause
Any cause of pericarditis
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Pericardial effusion clinical features
 Dyspnoea  ↑JVP (prominent x descent)  Bronchial breathing @ left base  Ewart’s sign: large effusion compressing left lower lobe  Signs of cardiac tamponade may be present.
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Investigations of pericardial effusion
 CXR: enlarged, globular heart ECG  Low-voltage QRS complexes  Alternating QRS amplitude (electrical alterans) Echo: echo-free zone around heart
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Management of pericardial effusion
Treat cause | Pericardiocentesis may be diagnostic and therapeutic use it for culture and cytology
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Cardiac tamponade definition
 Accumulation of pericardial fluid → ↑ intra-pericardial pressure → poor ventricular filling → ↓ CO
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Tamponade causes
``` any cause of pericarditis aortic dissection bacterial endocarditis warfarin trauma ```
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Signs of tamponade
 Beck’s Triad: ↓ BP, ↑ JVP, quiet heart sounds  Pulsus paradoxus: pulse fades on inspiration  Kussmaul’s sign = JVP rise on inspiration
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Investigations of tamponade
ECG - low voltage QRS - electrical alterans CXR - Large globular heart Echo - diagnostic - echo free zone around the heart
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Management of tamponade
 Urgent pericardiocentesis  20ml syringe + long 18G cannula  45degrees, just left of xiphisternum, aiming for tip of left scapula.  Aspirate continuously and watch ECG.  Treat cause  Send fluid for cytology, ZN stain and culture
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Acute myocarditis causes
Idiopathic - 50% Viral - cocksackie flu HIV Bacterial - staph aureus syphilis Drugs - Herceptin Phenytoin
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Acute myocarditis symptoms
Flu like prodrome-- sore throat myalgia dyspnoea fatigue chest pain Arrhythmias == palpitations
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Signs of acute myocarditis
Soft S1 | S4 gallop as atria contract to hard ventricles
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Investigations for acute myocarditis
ECG  ST-elevation or depression  T wave inversion  Transient AV block Bloods: +ve trop, ↑CK
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Hypertrophic obstructive cardiomyopathy causes
Left ventricular outflow tract obstruction due to asymmetrical septal hypertrophy Autosomal dominant inheritance B - myosin heavy chain mutation commonest Ask questions about family history of sudden death
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Symptoms of HOCM
Angina Dyspnoea Palpitations: AF, WPW, VT Exertional syncope or sudden death
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Signs of HOCM
Jerky pulse Double apex beat S4 sound Harsh early systolic murmur
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Investigations HOCM
ECG | -LVH
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Management of HOCM
Medical  -ve inotropes: 1st – β-B, 2nd –verapamil  Amiodarone: arrhythmias  Anticoagulate if AF or emboli Non-medical  Septal myomectomy (surgical or chemical) if severe symptoms Consider ICD
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Cardiac myxoma definition and cause
Rare benign cardiac tumour May be familial eg due to part of Carney Complex - cardiac myxoma - skin pigmentation - cushing's 90% found in Left atrium
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Features of cardiac myxoma
``` Clubbing fever weight loss signs similar to MS (MDM, systemic emboli and AF) but vary with posture ``` Diagnosed with echo Treatment with excision
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Restrictive cardiomyopathy causes
``` miSSHAPEN Sarcoid Systemic sclerosis Haemochromatosis Amyloidosis Primary - endoymyocardial fibrosis Eosinophilia Neoplasia == carcinoid ==> TR + PS ```
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Clinical features restrictive cardiomyopathy
``` Clinical features  RHF ̄c ↑JVP (prominent x and y descents)  Kussmaul’s sign: ↑JVP ̄c inspiration  Quiet heart sounds  S3  Hepatosplenomegaly  Ascites, oedema ``` this is the same as restrictive pericarditis
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Dilated cardiomyopathy causes
``` DILATE Dystrophy Infection Late pregnancy -- peri/post partum Autoimmune -- SLE Toxins - alcohol , doxorubicin Endocrine -- thryotoxicosis ```
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Presentation of dilated cardiomyopathy
LVF RVF Arrhythmias
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Signs of dilated cardiomyopathy
```  JVP ↑↑  Displaced apex  S3 gallop  ↓BP  MR/TR ```
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Investigations dilated cardiomyopathy
 CXR: cardiomegaly, pulmonary oedema  ECG: T inversion, poor progression  Echo: globally dilated, hypokinetic heart + ↓EF  Catheter + biopsy: myocardial fibre disarray
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Management dilated cardiomyopathy
 Bed rest  Medical: diuretics, ACEi, digoxin, anticoagulation  Non-medical: biventricular pacing, ICD  Surgical: heart Tx
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Bicuspid aortic valve manifestations
No problems at birth Most will eventually develop stenosis +- regurg Predisposes to infective endocarditis
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Atria septal defect definition
Hole connects the atria Secundum defects are commonest Often asymptomatic until adulthood LV compliance eventually gets worse so more blood in atria and gives L==> R shunt
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Signs and symptoms of Atrial septal defect
Symptoms: - dyspnoea - pulmonary HTN - arrhythmia - Chest pain ``` Signs:  AF  ↑JVP  Pulmonary ESM  PHT→TRorPR ```
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Complications of Atrial septal defect
``` Paradoxical emboli (ie from venous origin) Eisenmenger syndrome ```
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Investigations for Atrial septal defect
ECG: CXR: -pulmonary plethora, increased pulmonary perfusion due to the shunt Echo: -diagnostic
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Treatment for atrial septal defect
Transcatheter closure this is recommended if there is a lot of blood flowing from pulmonary to systemic (eisenmenger) 1.5:1 ratio due to cyanosis problems it needs management.
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Coarctation of the aorta definition
Congenital narrowing of the aorta usually just distal to the origin of the L subclavian artery M>F
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Associations of coarctation of the aorta with other diseases
Bicuspid aortic valve | Turner's syndrome
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Signs of coarctation of the aorta
Radio - femoral delay Weak femoral pulse Hypertension Systolic murmur -- bruit best heard over left shoulder
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Investigations for coarctation of aorta
CXR: - inferior rib notching ECG CT angiogram
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Treatment coarctation of aorta
Balloon dilatation and stenting
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Ventricular septal defect definition
Hole connecting the ventricles
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Causes of ventricular septal defect
Congenital Acquired post MI
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Presentation of ventricular septal defect
Either severe heart failure in childhood Or incidental finding in adulthood depending on severity
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Signs of VSD
 Small holes which are haemodynamically less significant → louder murmurs  Harsh, pansystolic murmur @ left sternal edge  Systolic thrill  Left parasternal heave  Larger holes → PHT
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Complications of VSD
infective endocarditis pulmonary hypertension eisenmenger's syndrome
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Investigations of VSD
ECG  Small: normal  Large: LVH + RVH CXR  Small: mild pulmonary plethora  Large: cardiomegaly + marked pulmonary plethora
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Treatment VSD
surgical closure if symptomatic VSD from large hole
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Tetralogy of fallot definition
VSD Pulmonary stenosis Right ventricular hypertrophy Overriding aorta The commonest congenital cyanotic heart disease occurs following abnormal separation of truncus arteriosus into aorta and pulmonary arteries Associated with DiGeorge syndrome CATCH-22 gene
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Presentation of fallot
 Infants: hypercyanotic episodes, squatting, clubbing Adult  Often asympto  Unoperated: cyanosis, EarlySystolicMurmur of PS  Repaired: dyspnoea, palpitations, RVF
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Fallot investigations
ECG: RVH + RBBB CXR: Coeur en sabot Echo: anatomy + degree of stenosis
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Treatment of fallot
surgically usually before age of 1 closure of VSD correction of pulmonary stenosis
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Marfan's syndrome epidemiology
Autosomal dominant M=F 1/5000
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Pathophysiology of marfan's syndrome
Mutation in FBN1 gene chromosome 5 - encodes fibrillin 1 glycoprotein fibrillin 1 is an essential component of elastin Histology gives cystic medial necrosis
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Presentation of Marfan's syndrome
Cardiac  Aortic aneurysm and dissection  Aortic root dilatation → regurgitation  MV prolapse ± regurgitation Ocular  Lens dislocation: superotemporal ``` MSK  High-arched palate  Arachnodactyly abnormal long and slender digits  Arm-span > height  Pectus excavatum  Scoliosis  Pes planus  Joint hypermobility ```
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Complications of marfan's
Ruptured aneurysms Spontaneous pneumothorax Diaphragmatic hernias Hernias
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Marfan's DDX
MEN-2B Homocystinuria Ehlers-danlos
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Investigations of Marfan's
 Slit-lamp examination: ectopia lentis CXR  Widened mediastinum  Scoliosis  Pneumothorax ECG  Arrhythmias: premature atrial and ventricular ectopics Echo  Aortic root dilatation → AR  MVP and MR  MRI: dural ectasia (dilation of neural canal)  Genetic testing: FBN-1 mutation
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Management of marfan's syndrome
 Refer to ortho, cardio and ophtho  Life-style alteration: ↓ cardiointensive sports  Beta-blockers slow dilatation of the aortic root  Regular cardiac echo  Surgery when aortic root ≥5cm wide
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Ehlers-Danlos syndrome pathogenesis
Rare heterogeneous group of collagen disorders 6 subtypes type 1&2 are commonest and autosomal dominant
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Presentation of ehlers danlos
 Hyperelastic skin  Hypermobile joints  Cardiac: MitralValveProlapse , AR, MR and aneurysms  Fragile blood vessels → easy bruising, GI bleeds  Poor healing
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Ehlers danlos syndrome DDX
Cutis laxa - loose skin and hypermobile joints pseudoxanthoma elasticum - skin laxity Marfan's syndrome