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Phase 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the different classes of cardiomyopathy?

A

Hypertrophic
Restrictive
Dilated
Arrhythmogenic right ventricular dysplasia

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2
Q

What causes hypertrophic cardiomyopathy?

A

Familial, with autosomal dominant inheritance

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3
Q

What causes restrictive cardiomyopathy?

A

Idiopathic

Secondary: amyloidosis, endomyocardial fibrosis

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4
Q

What are causes of dilated cardiomyopathy?

A 
Ischaemic
Idiopathic
Familial-genetic
Toxic (e.g. alcoholic)
Valvular
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5
Q

What are causes of arrhythmogenic right ventricular dysplasia?

A

Unknown

Familial, usually autosomal dominant inheritance, with incomplete penetrance

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6
Q

What is often mutated in hypertrophic cardiomyopathy?

A

Beta myosin heavy chain gene

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7
Q

What is the most common cause of sudden death in the young?

A

Hypertrophic cardiomyopathy

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8
Q

What is the annual mortality rate in hypertrophic cardiomyopathy?

A

1%

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9
Q

What complications can cause increased mortality rates in hypertrophic cardiomyopathy?

A

Sudden death
Progressive heart failure
AF with embolic stroke

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10
Q

What ECG findings are suggestive of left ventricular hypertrophy and may suggest hypertrophic cardiomyopathy?

A

Large QRS complexes
ST depression
Deep T inversion
Or non-specific changes

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11
Q

What is sokolow Lyon criteria?

A

S wave in V1 and R wave in V5 or V6 > 35mm

Criteria for determining LVH

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12
Q

How is hypertrophic cardiomyopathy diagnosed?

A

Echo: detecting otherwise unexplained left ventricular wall thickening in the presence of a non-dilated cavity, no valvular problem

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13
Q

What clue in the family history might suggest hypertrophic cardiomyopathy?

A

Sudden cardiac death in the family

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14
Q

What are the aims of management of hypertrophic cardiomyopathy?

A

Symptom treatment
Prevention of progression
Reduction in risk of sudden death

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15
Q

What are the medical management steps for hypertrophic cardiomyopathy?

A

Reduce gradient across LVOT by stepwise, progressive anti-hypertensives
Beta blocker: reduces LV contractility, reduces myocardial ischaemia and O2 demand
Calcium channel blockers (particularly Verapamil)
Amiodarone (to prevent arrhythmia)
Caution with diuretics (keep pt. well hydrated, prevent collapse)

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16
Q

Which patient’s would be considered for non medical management of their hypertrophic cardiomyopathy?

A

Marked LVOT gradient >50 mmHg (despite Rx)
Severe exertional dyspnea
Chest pain and exertional syncope
Refractory to max medical Rx

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17
Q

What is the non medical management for hypertrophic cardiomyopathy?

A

RV pacing (RV excited first, pulling the LVOT mass, preventing obstruction), no reduction in mortality or sudden death
ICD: Life saving, superior to AAD, Prevents sudden death. Patients at high risk (primary prevention) or with previous arrhythmia (seconday)
Surgical septal myomectomy +/- mitral valve replacement
Catheter septal ablation (ethanol)

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18
Q

What lifestyle advice should be offered to patients with hypertrophic cardiomyopathy?

A 
Avoid stressful physical situation or competitive sport 
(non-competitive recreational sports activities, not believed to be contraindicated) 
CPR education (family members), psychosocial counselling
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19
Q

What is dilated cardiomyopathy?

A

Progressive disease of heart muscle characterised by LV enlargement and LVEF impairment with normal wall thickness
(ischaemic DCM: thinned walls)

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20
Q

What are the different types of dilated cardiomyopathy?

A 
Ischaemic: most common (60%)
Idiopathic (genetic)
Acute viral myocarditis
Toxic cardiomyopathy 
Valvular heart disease
Metabolic and endocrine causes (e.g thyrotoxicosis)
Peripartum (1 month pre-, 5 month postpartum)
Tachycardia-induced cardiomyopathy
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21
Q

What investigations should be done for dilated cardiomyopathy?

A 
Full blood count
Thyroid function tests
Cardiac biomarkers
B-type natriuretic peptide assay
Electrocardiography (ECG)
Chest radiography
Echocardiography
Cardiac MRI
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22
Q

What are medical treatment options for dilated cardiomyopathy?

A 
ACE inhibitors/ARB
Beta-blockers
MRA (Aldosterone antagonists) 
Diuretics
Ivabradine (inhibit funny channel, slow HR)
Digoxin
Antiarrhythmics
Anti-coagulation (in case of AF)
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23
Q

What are non medical treatment options for dilated cardiomyopathy?

A

CRT (cardiac resynchronisation therapy) wide QRS
(LBBB >120 ms, non-LBBB >150 ms)
ICD (implantable cardioverter defibrillator)
LV assist device - temporary until heart transplant
Heart Transplant

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24
Q

How does cardiac resynchronisation therapy work for dilated cardiomyopathy?

A

In DCM, septum contracts first, outer wall takes longer to receive signal so it contracts desynchronously
CRT works to synchronise contraction and pump more efficiently

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25
Q

What lifestyle advice should be offered to patients with dilated cardiomyopathy?

A

Diet: sodium and water restrictions
Moderate exercise: keep fit, cardiovascular training, deconditioning is a very common cause of dyspnea
Cardiac rehabilitation improves patient outcomes
Psych. Counseling, pt. education

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26
Q

What is restrictive cardiomyopathy?

A

Restrictive filling and reduced diastolic volume of either or both ventricles, with normal or near-normal systolic function

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27
Q

What are some primary and secondary causes of restrictive cardiomyopathy?

A

Primary: endomyocardial fibrosis, Löffler’s endocarditis, idiopathic restrictive cardiomyopathy
Secondary: infiltrative diseases (amyloidosis, sarcoidosis, radiation carditis), storage diseases (haemochromatosis, glycogen storage disorders, Fabry’s disease)

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28
Q

What is Loefflers endocarditis?

A

Form of restrictive cardiomyopathy which affects endocardium
Occurs with white cell proliferation, eosinophils

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29
Q

What is Fabrys disease? What problems occur?

A 
X linked lysosomal storage disease 
Pain
Kidney disease
Hypertension
Restrictive cardiomyopathy 
Angiokeratomas 
Anhydrosis 
Raynauds
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30
Q

What causes primary cardiac amyloidosis?

A

Overproduction of light chain IG from a monoclonal population of plasma cells, usually associated with multiple myeloma

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31
Q

What causes secondary cardiac amyloidosis?

A

Chronic inflammatory conditions such as Crohn’s disease, rheumatoid arthritis, tuberculosis, and familial Mediterranean fever

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32
Q

What types of cardiac amyloidosis are there?

A

Primary
Secondary
Familial
Senile

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33
Q

What is haemochromatosis?

A

Iron overload and deposition of iron in sarcoplasmic reticulum of many organs, including heart

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34
Q

What is the inheritance pattern of haemochromatosis?

A

Autosomal recessive

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35
Q

What is the treatment for haemochromatosis?

A

Repeated phlebotomy

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36
Q

What is cardiac sarcoidosis?

A

Formation of non-caseating granulomas that can infiltrate the myocardium

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37
Q

What percent of people with sarcoidosis get restrictive cardiomyopathy?

A

5%

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38
Q

What other problems is cardiac sarcoidosis associated with?

A

Lymphadenopathy
Skin rashes
Splenomegaly

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39
Q

What can cardiac sarcoidosis (restrictive cardiomyopathy) progress to?

A

Dilated cardiomyopathy

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40
Q

What is treatment for cardiac sarcoidosis? What is a potential problem?

A

Steroids
Might cause scar tissue
AV block, sinister arrhythmia and Sudden death is not prevented by steroids, hence ICD preferable

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41
Q

What characterises arrhythmogenic right ventricular cardiomyopathy?

A

Patchy apoptosis of the right and, to a lesser extent, left ventricles
Fat cardiomyopathy because of fatty infiltration of right ventricle

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42
Q

In what proportion of patients is arrhythmogenic right ventricular cardiomyopathy familial? What mode of inheritance?

A

50%

Autosomal dominant

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43
Q

When does arrhythmogenic right ventricular cardiomyopathy present and with what problems?

A

Early adulthood
Supraventricular and ventricular arrhythmias
Right-sided heart failure
Sudden death

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44
Q

What would you expect to see on an ECG of a patient with arrhythmogenic right ventricular cardiomyopathy?

A 
Epsilon waves (slurred ST segments) V1-3
Inverted T waves V2, V3 in absence of right bundle branch block
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45
Q

What would you expect to see on an echo of a patient with arrhythmogenic right ventricular cardiomyopathy?

A

Localised RV aneurysm, isolated RV failure

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46
Q

What would you expect to see on MRI and histology of a patient with arrhythmogenic right ventricular cardiomyopathy?

A

Fatty infiltration of right ventricle

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47
Q

What symptoms/problems do cardiomyopathies usually present with?

A 
Heart failure: SOB, ankle swelling 
Arrhythmia
Sudden death
Chest pain 
Incidental finding on screening
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48
Q

What is angina?

A

Blood perfusion of myocardium, through coronaries is not enough
Provoked by increased demand, or reduced supply

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49
Q

Which syndromes fit under the criteria of ACS?

A

Unstable angina
NSTEMI
STEMI

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50
Q

Around what percentage diameter closure of a coronary artery is enough to start to cause symptoms?

A

70%

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51
Q

How does coronary atherosclerosis lead to a STEMI?

A

Atherosclerotic plaque forms with fibrous cap - angina
Cap ruptures - NSTEMI
Blood clot forms around the rupture, blocks the artery - STEMI

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52
Q

Describe how you clinically distinguish between angina, NSTEMI and STEMI

A

Stable angina: coronary circulation insufficient on exertion,
pain on exertion
Unstable angina: circulation insufficiency even on rest, angina pain at rest, or crescendo nature, no myocardial damage
NSTEMI: circulation insufficient enough to cause myocardial necrosis.
Raise in Troponin, With or without ECG changes
STEMI: Transmural myocardial damage. ECG changes

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53
Q

What features allow you to make a clinical diagnosis of angina pectoris?

A

Age
Male
Cardiovascular risk factors including: Smoking, Diabetes, Hypertension, Dyslipidaemia, Family history of premature CAD, Other cardiovascular disease (erectile dysfunction, PVD, stroke), History of established CAD

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54
Q

What is typical anginal chest pain?

A

Constricting discomfort in front of chest, neck, shoulders, jaw, or arms
Precipitated by physical exertion
Relieved by rest or GTN within about 5 minutes

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55
Q

If you are 10-30% suspicious of chest pain as being CAD, what imaging would you do?

A

CT
Calcium scoring
+/- CT coronary angiogram

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56
Q

If you are 30-60% suspicious that chest pain is cardiac in origin, what imaging would you do?

A

Functional imaging:
Stress echocardiography - Pharmacological (Dobutamine stress echo) or physical
Myocardial perfusion scan
Cardiac magnetic resonance stress test

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57
Q

What is myocardial perfusion imaging?

A

Non-invasive imaging test that shows how well blood perfuses
myocardium
Can show areas of heart muscle that aren’t getting enough blood flow. Also known as nuclear stress test

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58
Q

If you are 60-90% suspicious that chest pain is cardiac in origin, what imaging do you do?

A

Invasive coronary angiography

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59
Q

What are the 3 major risk factors for angina pectoris?

A

Diabetes
Smoking
Hyperlipidaemia (tot. chol > 6.47 mmol/litre)

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60
Q

What should be given as soon as a diagnosis of unstable angina or NSTEMI is made?

A

Aspirin and antithrombin

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61
Q

After diagnosing unstable angina or NSTEMI, what tool would you use to assess individual risk of future adverse cardiovascular events using an established risk scoring system that predicts 6-month mortality?

A

Global Registry of Acute Cardiac Events [GRACE]

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62
Q

What is the initial management for ACS absolute requirements?

A 
Dual Anti-platelets: aspirin, clopidogrel, Ticagrelor, prasugrel
Heparin (LMWH) 
Beta blocker
Statin (high dose Atorvastatin)
ACE inhibitor
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63
Q

What are additional ACS management steps which can be taken on top of the absolute requirements?

A

Nitrates
Morphine
Oxygen
IIb/IIIa inhibitors (stronger anti-platelets)

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64
Q

What drugs should be considered as part of the early management for patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-
month mortality above 3.0%), and who are scheduled for angiography within 96 hours of admission?

A

IV eptifibatide or tirofiban (Glycoprotein IIb/IIIa inhibitors)

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65
Q

What should risk stratification for an NSTEMI include?

A

Full clinical history (age, previous MI, PCI or CABG)
Physical examination (BP, HR)
Resting 12-lead ECG (dynamic or unstable patterns that indicate myocardial ischaemia)
Blood tests (troponin I or T, creatinine, glucose and haemoglobin)

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66
Q

Which NSTEMI patients should be offered angiography within 96h of first admission?

A

Intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%) if they have no contraindications to angiography (such as active bleeding or comorbidity)
As soon as possible for patients who are clinically unstable or at high ischaemic risk

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67
Q

A 23 year old man who is a know IVDU is referred to MAU. He has a 4 day Hx of malaise, fever and lethargy. On examination his temp is 38.3, pulse 114 regular, resp rate 24, BP 102/64 and Sats 94% on air. Cardiac auscultation reveals a pansystolic murmur heard best at left lower sternal edge, which was not present when he attended the ED 4 months previously. What is the most important diagnosis to consider in this pt?

A

Infective endocarditis

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68
Q

Cardiac auscultation reveals a pansystolic murmur heard best at left lower sternal edge. What valvular abnormality do the auscultation findings indicate?

A

Tricuspid regurgitation

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69
Q

What pulmonary condition is a patient with infective endocarditis at risk of?

A

Pulmonary abscess
Septic emboli
Pulmonary infective seeding
Pulmonary embolism

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70
Q

What 2 investigations are most important in confirming a diagnosis of infective endocarditis?

A

Echo

Blood cultures

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71
Q

A 23 year old man who is a know IVDU is referred to MAU. He has a 4 day Hx of malaise, fever and lethargy. On examination his temp is 38.3, pulse 114 regular, resp rate 24, BP 102/64 and Sats 94% on air. Cardiac auscultation reveals a pansystolic murmur heard best at left lower sternal edge, which was not present when he attended the ED 4 months previously. What investigations are appropriate in this patient?

A 
Echo
Blood cultures
ECG
CXR
FBC
CRP/ESR
U and Es
ABG
Lactate
LFTs
Clotting
Hepatitis screen
HIV test
Urine culture
Urinalysis 
CT thorax
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72
Q

What is the most common causative infective organism in bacterial endocarditis?

A

Staphylococcus aureus

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73
Q

Which MI can cause an associated transient complete heart block? And why?

A

Inferior due to right coronary artery supplying AV node

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74
Q

In a patient being treated for an MI, what might be features that they have decompensated and are having further problems?

A

Hypotension <90 systolic
Loss of consciousness
Chest pain
Shortness of breath

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75
Q

What is the management for a bradycardic peri arrest?

A

Atropine 500 mcg aliquots up to 3mg
Isoprenaline and adrenaline infusion
Transcutaneous pacing

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76
Q

How is amaurosis fugax investigated?

A

Carotid Doppler
ECG - AF
Echo - source of embolism

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77
Q

What is the management for acute heart failure?

A

Sit patient upright
High flow oxygen
IV access and monitor ECG
Treat any arrhythmias
Diamorphine 1.25-5mg IV slowly (caution in liver failure and COPD)
Furosemide 40-80mg IV slowly (larger dose if renal failure)
GTN spray 2 puffs SL or 2x 0.3mg tablet SL (not if systolic <90)
If systolic >100, nitrate infusion - isosorbide dinitrate 2-10mg/h
IVI keep systolic >90
If patient worsening - further dose furosemide 40-80mg
Consider CPAP
Increase nitrate infusion if able without drop in systolic
If systolic <100 treat as cardiogenic shock and refer to ICU

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78
Q

How does coarctation of the aorta present?

A 
Headache
Epistaxis 
Cold extremities 
Claudication 
HTN 
Mid systolic murmur over anterior chest, back and spinous process
Or continuous murmur
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79
Q

What radiological finding is indicative of coarctation of the aorta?

A

Notching of ribs due to erosion by collaterals

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80
Q

What are some causes of a raised JVP?

A

Right sided/congestive heart failure
Pulmonary HTN/PE
Severe asthma
Excessive fluid retention e.g. Cirrhosis

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81
Q

What is initial management for a patient with a narrow complex SVT who is not haemodynamically compromised?

A

IV adenosine in absence of contraindication e.g. Asthma
This may terminate the tachycardia or cause sufficient slowing in rate to allow identification of underlying rhythm to guide optimal anti arrythmic therapy

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82
Q

What is initial management for a patient with a narrow complex SVT who is haemodynamically compromised (chest pain, hypotension, systolic <90, evidence of cardiac failure)?

A

DC cardioversion

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83
Q

What pulse rate is suggestive of SVT?

A

Greater than 160

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84
Q

What pulse rate is suggestive of an accessory pathway in the heart?

A

Greater than 200

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85
Q

What are treatment options for SVT?

A

IV adenosine
Carotid sinus massage/vagal manoeuvres
DC cardioversion

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86
Q

A 72 year old man with ischaemic heart disease complains of feeling faint for past hour. He is pale, sweaty and hypotensive. His ECG shows a regular tachycardia of 180 with QRS duration of 0.2 secs. What is the most appropriate treatment? Why?

A

DC cardioversion

In VT - broad complex tachy

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87
Q

A 64 year old woman with known AF treated with digoxin attends surgery complaining of transient loss of vision in left eye which recovered spontaneously. What did she have and what should you do now?

A

Amaurosis fugax

Requires anticoagulation - warfarin

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88
Q

A 73 year old man with known carcinoma of the bronchus becomes increasingly short of breath over the past few days. The chest X-ray shows and enlarged heart shadow but no pulmonary oedema. What is the diagnosis and what needs to be done about it?

A

Pericardial effusion

Pericardiocentesis

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89
Q

Does inspiration exacerbate left or right sided murmurs? Why?

A

Right

Increases venous return to the heart

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90
Q

What are some causes of AF?

A 
Thyrotoxicosis
Mitral stenosis
Ischaemic heart disease
Congenital heart disease 
Alcohol/caffeine/tobacco
HTN
Pneumonia
Asthma/COPD
PE
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91
Q

A 70 year old man complains of increasing dyspnoea over months. He has had to give up playing squash. An ECG shows AF and right ventricular hypertrophy and strain. Multiple small filling defects are seen on CTPA. What is the single next most appropriate step in management?

A

Anticoagulation

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92
Q

A 55 year old man presents six weeks after an MI with fatigue and fever. On examination he has a soft systolic sound over the left fourth intercostal space next to the sternum which is loudest when leaning him forward. What does he have and what sound are you hearing?

A

Dressler’s syndrome with a pericarditis

Hearing pericardial rub

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93
Q

What are the characteristic features of Dressler’s syndrome?

A

Pleuritic chest pain
Low grade fever
Pericarditis

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94
Q

How do you treat Dressler’s syndrome?

A

NSAIDs

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95
Q

A 65 year old female presents 6 weeks after MI with deteriorating SOB of relatively recent onset. On examination there is a soft first heart sound followed by a mid systolic murmur which is loudest at the apex and in expiration. What does she have?

A

Mitral regurgitation or prolapse due to dysfunction of the papillary muscles following MI

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96
Q

A 72 year old female presents with deteriorating shortness of breath. On auscultation of the heart there is a loud first heart sound and a rumbling mid diastolic murmur. What is it?

A

Mitral stenosis

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97
Q

What is the main cause of mitral stenosis?

A

Rheumatic heart disease

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98
Q

What dietary advice should be offered to patients post MI?

A

Avoid high saturated fat content - cheese, milk, fried food
Switch to high fibre, starch based food
5 portions fruit and veg and oily fish

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99
Q

Which wave of the jugular venous waveform is associated with closure of the tricuspid valve?

A

C wave

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100
Q

What are some examples of duct dependent congenital heart disease?

A

Aortic coarctation
Critical aortic stenosis
Truncus arteriosus
Hypoplastic left heart syndrome

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101
Q

An 11 day old baby presents with poor feeding and breathlessness. She was born at 37 weeks weighing 2.7kg by elective c section. She has never fed well but had deteriorated markedly on the day of admission. On examination she is responding to pain, mottled and has a tympanic temp of 34.6. Her heart rate is 130 with impalpable pulses and gallop rhythm. Her resp rate is 40 with marked recession. She has a 4cm liver. Her sats and BP are unrecordable. She has obvious central cyanosis. What is the most likely mechanism of shock?

A

Duct dependent congenital heart disease

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102
Q

What are risk factors for major artery embolism (axillary, brachial)?

A 
AF
Rheumatic heart disease
Previous MI
Aneurysm 
Atheromatous thrombosis
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103
Q

What drugs do you put a patient on for secondary prevention after an MI?

A

ACEi
Dual anti-platelet therapy: aspirin 75mg OD, clopidogrel
Beta blocker
Statin

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104
Q

At what intervals do you measure trop T if you suspect an MI?

A

At symptom onset
6-12 hours after assessment
Up to 24 hours after

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105
Q

What ECG changes occur in hyperkalaemia?

A

Peaked T waves particularly in precordial leads
Widened QRS when potassium is >6.5
Decreased p wave amplitude
Increased PR interval
Bradycardia and AV block if potassium >7
P waves lost and sine wave - fatal arrhythmia

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106
Q

What ECG changes are associated with pericarditis?

A

Concave upward ST segment elevation

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107
Q

What are causes of prolonged QT?

A

Congenital prolonged QT: Loon-Ganong-Levine syndrome
Hypocalcaemia
Drugs: Amiodarone, sotalol

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108
Q

What is a Carey Coombes murmur?

A

Mid diastolic rumble but no opening snap

Mitral valve thickening in rheumatic heart disease

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109
Q

In Marfans and hereditary causes of aortic aneurysm, what is the underlying pathology?

A

Cystic medial necrosis

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110
Q

A 26 year old female is admitted with palpitations. ECG shows a shortened PR interval and wide QRS complexes associated with slurred upstroke in lead II. What is the definitive management of this condition? What is the other alternative?

A

Accessory pathway radiofrequency ablation to treat Wolff Parkinson white syndrome
Sotalol (if no AF)
Amiodarone
Flecainide

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111
Q

What is the difference between type A and B wolff Parkinson White syndrome?

A

Type A: left sided pathway. Dominant R wave in V1

Type B: right sided pathway. No dominant R in V1

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112
Q

What are associations of WPW?

A 
HOCM
Mitral valve prolapse 
Ebsteins anomaly 
Thyrotoxicosis
Secundum ASD
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113
Q

What is Ebsteins anomaly?

A

Congenital defect in which septal and posterior leaflets of tricuspid valve are displaced towards the apex of the right ventricle

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114
Q

What is current guidance on the use of aspirin in patients who have ischaemic heart disease? How does this vary for other forms of cardiovascular disease (stroke, PAD)?

A

All patients should take aspirin if there is no contraindications
Other forms should be offered clopidogrel first line

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115
Q

How does aspirin work as an anti platelet?

A

Blocks cyclooxygenase 1 and 2

This prevents thromboxane A2 formation and therefore reduces ability of platelets to aggregate

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116
Q

A 51 year old female presents to ED following episode of transient weakness lasting 10-15 mins. Examination reveals that the patient is in AF. If the patient remains in AF what is the most suitable form of anticoagulation? Why?

A

Warfarin with target INR 2-3

CHA2DS2VASc score 2 for TIA, 1 for being female

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117
Q

What are the criteria of CHA2DS2VASc?

A 
Congestive heart failure - 1
Hypertension - 1
Age over 75 - 2, 65-74 - 1
Diabetes - 1
Stroke or TIA - 2
Vascular disease - 1
Sex female - 1
Score 1: male consider anticoagulation, females no treatment
Score 2 or more: offer anticoagulation
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118
Q

What is the HASBLED scoring system?

A 
Risk assessment of warfarinisation
Hypertension >160 - 1
Abnormal renal function dialysis or creatinine >200 - 1
Abnormal liver function cirrhosis, bilirubin >2x, enzymes >3x -1
Stroke - 1
Bleeding
Labile INR, time in range <60% - 1
Elderly over 65 - 1
Drugs predisposing to bleeding - 1
Alcohol over 8 units a week -1
Score 3 or more, high risk bleeding
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119
Q

A 30-year-old male is stabbed outside a nightclub. He has a brisk haemoptysis and in casualty has a chest drain inserted into the left chest. This drained 750ml frank blood. He fails to improve with this intervention. He has received 4 units of blood. His CVP is now 13 mmHg (normal range 3-8). What needs to be done now?

A

Pericardiocentesis - he has cardiac tamponade

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120
Q

What is becks triad?

A

Elevated venous pressure, reduced arterial pressure, reduced heart sounds - cardiac tamponade

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121
Q

What is a slow rising pulse a sign of?

A

Aortic stenosis
Ejection systolic murmur that radiates to the carotids
Obstruction to outflow - narrow pulse pressure

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122
Q

What is Eisenmengers syndrome?

A

Right to left shift associated with deteriorating pulmonary hypertension and RV overload in conditions such as large ventricular septal defects

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123
Q

What murmur is associated with sero-negative arthopathies such as ankylosing sponylitis?

A

Aoritc regurgitation

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124
Q

What is syphilitic aortitis?

A

Inlammation of aorta associated with tertiary syphilis. SA begins as inflammation of outermost layer of the blood vessel, including vasa vasorum. As SA worsens, the vasa vasorum undergo hyperplastic thickening, restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall. Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm with associated aortic regurgitation

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125
Q

What are J waves pathognomonic of?

A

Hypothermia

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126
Q

What are some causes of QT prolongation?

A

Hypothermia
Congenital prolonged QT: Romano-ward syndrome, Jervell and Lange-Nielsen syndrome
Hypocalcaemia
Drug therapy: amiodarone, sotalol, TCAs, SSRIs, methadone, chloroquine, erythromycin, haloperidol

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127
Q

What are ECG features of pulmonary embolism?

A 
Sinus tachycardia
Right heart strain
Right axis deviation
S1 Q3 T3 
Right bundle branch block
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128
Q

When is a U wave prominent on ECG?

A

Hypokalaemia

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129
Q

An 8 year old girl presents with loss of consciousness and occasional awareness of heartbeat. She has been deaf from birth. What syndrome might she have?

A

Jervell-Lange-Neilson variant of long QT syndrome

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130
Q

What is Jervell and Lange-Nielsen syndrome?

A

Type of long QT syndrome associated with severe bilateral sensorineural hearing loss

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131
Q

What is Romano Ward syndrome?

A

Major variant of long QT syndrome

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132
Q

What are some causes/associations of AF?

A 
Thyrotoxicosis
Mitral valve disease
Congenital heart disease
Previous cardiac surgery
Pericarditis
Ishaemic heart disease
Pulmonary embolism
Pneumonia
Sepsis
Alcohol
Excess caffeine
Cardiomyopathy
Sleep apnoea
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133
Q

What drugs do you use to chemically cardiovert someone in AF?

A

Amiodarone and flecainide

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134
Q

When is chemical cardioversion used for AF?

A

When patient is stable

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135
Q

What are features of severe aortic stenosis?

A 
Narrow pulse pressure
Slow rising pulse
Delayed ejection systolic murmur
Soft/absent S2
S4
Thrill
Duration of murmur 
Left ventricular hypertrophy or failure
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136
Q

What are causes of aortic stenosis?

A 
Degenerative calcification
Bicuspid aortic valve
Williams syndrome (supravalvular stenosis)
Post rheumatic disease
Subvalvular: HOCM
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137
Q

What is the management for aortic stenosis?

A

Asymptomatic: observe
Symptomatic: valve replacement
Asymptomatic but valvular gradient >40 and features of left systolic dysfunction: consider surgery
Balloon valvuloplasty limited to patients with critical aortic stenosis who are not fit for replacement

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138
Q

What are the 2 types of VT?

A

Monomorphic: commonly caused by MI
Polymorphic: can be torsades de pointed precipitated by prolonged QT

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139
Q

What is the management for VT?

A

If patient has adverse signs: systolic <90, chest pain, heart failure, pulse >150 then immediate cardioversion
If stable: anti arrhythmics - amiodarone through central line, lidocaine, procainamide. If these fail then electrical cardioversion

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140
Q

What is the acute management of SVT?

A

Vagal manoeuvres - valsalva
IV adenosine 6mg then 12mg then 12mg (not in asthmatics, verapamil)
Electrical cardioversion

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141
Q

What can be used to prevent episodes of SVT?

A

Beta blockers

Radio frequency ablation

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142
Q

What do NICE guidelines on STEMI say about transfer to another centre for provision of PCI?

A

Primary PCI should be offered to all patients who present within 12 hours of onset of symptoms if it can be delivered within 120 mins of the time when fibrinolysis could have been given
If the ECG after 90 mins of fibrinolysis doesn’t show resolution, they require transfer for PCI

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143
Q

Which pulse abnormality is associated with asthma and pericardial tamponade?

A

Pulsus paradoxus
Natural obstruction to flow from the lungs to LV during inspiration is enhanced
Pulse pressure falls during inspiration (over 20mmHg)

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144
Q

Which heart defects are associated with turners syndrome?

A

Bicuspid aortic valve

Coarctation of the aorta

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145
Q

What is the most appropriate investigation for suspected bacterial endocarditis?

A

Blood cultures

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146
Q

What are the risk factors used to calculate a CHA2DS2 VASc score?

A 
Congestive heart failure
Hypertension
Age >75 (2), 65-74 (1)
Diabetes
Stroke or TIA
Vascular disease 
Sex (female)
Score 1: males consider anticoagulant 
2 or more: offer anticoagulation
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147
Q

What are features of bacterial endocarditis?

A

Fever
Breathlessness
Irregular pulse
New murmur

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148
Q

What are some normal variants on an ECG?

A

Sinus arrhythmia
Right axis deviation in tall thin people
Left axis deviation in short obese people
Partial right bundle branch block

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149
Q

What are some variants which may be seen on an ECG of an athlete due to high vagal tone?

A

Sinus bradycardia
1st degree AV block
Wenckebach phenomenon (2nd degree AV block Mobitz 1)
Junctional escape rhythm

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150
Q

Which beta blockers have been shown to reduce mortality in stable heart failure?

A

Carvedilol and bisoprolol

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151
Q

Which drugs have been shown to improve mortality in patients with chronic heart failure?

A

ACE inhibitors
Spironolactone
Beta blockers
Hydralazine with nitrates

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152
Q

What are management options for heart failure?

A

First line: ACE inhibitor and beta blocker
Second line: aldosterone antagonist, ARB or hydralazine with nitrate
If symptoms persist: cardiac resynchronisation therapy or digoxin, ivabradine
Diuretics for fluid overload
Annual influenza vaccine
One off pneumococcal vaccine

153
Q

A 45 year old cattle farmer presents with 2 month Hx of increasing fatigue, SOB and night sweats. On admission he is pyrexial with a temp of 39.7 and a new early diastolic murmur on auscultation. What is the diagnosis? What investigation is required to confirm this?

A

Bacterial endocarditis

Echo

154
Q

What is the most common cause of infective endocarditis?

A

Staphylococcus aureus

155
Q

What is the strongest risk factor for developing infective endocarditis?

A

Previous episode of endocarditis

156
Q

What is the most common cause of endocarditis in patients following prosthetic valve surgery?

A

Staphylococcus epidemidis

157
Q

What are ECG findings with atrial flutter?

A

Sawtooth appearance
Underlying atrial rate 300, 2:1 AV block - ventricular rate 150
Flutter waves visible following carotid sinus massage or adenosine

158
Q

What is the management for atrial flutter?

A

Similar to AF
More sensitive to cardioversion so lower energy levels may be used
Radiofrequency ablation of tricuspid valve isthmus curative for most patients

159
Q

Which agents are used to control rate in patients with AF?

A

Beta blockers
Calcium channel blockers
Digoxin (preferred choice if also has heart failure)

160
Q

Which agents are used for rhythm control in AF?

A

Sotalol
Amiodarone
Flecainide

161
Q

Which factors favour rate control for AF?

A

Older than 65
History of ischaemic heart disease
Contraindications to antiarrrhythmic drugs
Unstable for cardioversion

162
Q

What are acute management options for acute heart failure?

A 
Oxygen 
Diuretics
Opiates
Vasodilators
Inotropic agents
CPAP
Ultrafiltration 
Mechanical circulatory assistance
163
Q

Which factors favour rhythm control in AF?

A 
Younger than 65
Symptomatic 
First presentation
Lone AF or secondary to a corrected precipitant
Congestive heart failure
164
Q

What are the different types of AF?

A

Acute: onset in previous 48 hours
Paroxysmal: spontaneous termination within 7 days
Recurrent: two or more episodes
Persistent: not self terminating, lasting longer than 7 days or prior cardioversion
Permanent: long standing AF over 1 year, not terminated by cardioversion

165
Q

What do NICE guidelines recommend for management of unstable angina and NSTEMI?

A

Aspirin 300mg
Nitrates or morphine to relieve chest pain
Antithrombin: enoxaparin/fondaparinux if not high risk bleeding and not having angiography. Unfractioned heparin
Clopidogrel 300mg for 12 months

166
Q

Who should be offered coronary angiography with unstable angina and NSTEMI?

A

Considered within 96 hours of first admission to hospital who have predicted mortality above 3%
ASAP in those who are clinically unstable

167
Q

A 45 year old man presents with palpitations that began around 40 mins ago, other than a stressful day at work there appears to be no obvious trigger. He denies chest pain or dyspnoea. An ECG shows regular tachycardia of 180 bpm with QRS duration 0.1s. BP is 106/70 and sats are 98%. You ask him to valsalva but this has no effect. What is the most appropriate next course of action?

A

IV adenosine: 6mg then 12mg then 12mg (not in asthmatics)

Electrical cardioversion if this fails

168
Q

What is first line treatment for heart failure?

A

ACE inhibitor and beta blocker

169
Q

What is second line treatment for heart failure?

A

Aldosterone antagonist
Angiotensin II receptor blocker
Hydralazine in combination with a nitrate

170
Q

If symptoms of heart failure persist despite first and second line therapies, what should be considered?

A

Cardiac resynchronisation therapy
Digoxin
Ivabridine if: already on suitable therapy, HR >75, left ventricular fraction <35%

171
Q

What should be given to treat fluid overload in heart failure?

A

Diuretics

172
Q

What is first line therapy for stable angina?

A

Beta blocker or calcium channel blocker or combo of 2

173
Q

What is Kussmauls sign? What is it a feature of?

A

JVP increasing with inspiration

Feature of constrictive pericarditis

174
Q

What are causes of pericarditis?

A

Viral: coxsackie, echovirus, Epstein Barr, influenza, HIV, mumps
Bacterial: staph, haemophilus, pneumococcus, salmonella, TB, meningococcus, syphilis
Rheumatological: sarcoidosis, SLE, RA, dermatomyositis, scleroderma, polyarteritis nodosa, vasculitis, ank spond
Drugs: procainamide, hydralazine, isoniazid, phenytoin
Uraemia
MI/dresslers syndrome

175
Q

How does pericarditis present?

A

Chest pain radiating to neck/shoulders
Aggravated by inspiration, swallowing, coughing, lying flat
Relieved by sitting up and leaning forward
Non productive cough
Chills
Weakness

176
Q

What are signs of pericarditis?

A

Pericardial friction rub, louder in inspiration
Tachypnoea
Tachycardia
Fever
Dyspnoea
Orthopnoea
Pulses paradoxus (decrease in SBP in inspiration)

177
Q

What are the 4 stages of ECG changes seen in pericarditis?

A

Stage 1: diffuse concave upward ST elevation with concordance of T waves
Stage 2: ST segments return to baseline, t wave flattening
Stage 3: t wave inversion
Stage 4: gradual resolution of t wave inversion
Tamponade: electrical alternans

178
Q

What investigations should be done for pericarditis?

A 
ECG
CXR
FBC
ESR and CRP
U and Es
Cardiac enzymes 
Blood cultures
Tuberculin test and sputum for AFB
Antistreptolysin titre
RF, ANA, anti DNA 
Thyroid function
HIV, coxsackie, influenza, echovirus antibodies 
Pericardial biopsy 
Echo if tamponade
179
Q

What are features of constrictive pericarditis?

A 
Dyspnoea 
Right heart failure: elevated JVP, ascites, oedema, hepatomegaly 
JVP shows prominent x and y descent 
Pericardial knock - loud S3
Kussmauls sign positive
180
Q

What are differences between cardiac tamponade and constrictive pericarditis?

A

Tamponade: absent Y descent, pulsus paradoxus
Pericarditis: X and Y descent, Kussmauls sign, pericardial calcification on CXR

181
Q

What are causes of ejection systolic murmurs?

A 
Aortic stenosis 
Pulmonary stenosis
Hypertrophic obstructive cardiomyopathy
Atrial septal defect
Fallots
182
Q

What are causes of pan systolic murmurs?

A

Mitral/tricuspid regurgitation

VSD

183
Q

What are causes of late systolic murmurs?

A

Mitral valve prolapse

Coarctation of aorta

184
Q

What are causes of an early diastolic murmur?

A

Aortic regurg

Graham steel murmur (pulmonary regurg)

185
Q

What is a cause of a continuous machinery like murmur?

A

Patent ductus arteriosus

186
Q

In which patient groups should Q risk not be used?

A

85 and older
Type 1 diabetes
eGFR less than 60/albuminuria
History of familial hyperlipidaemia

187
Q

With what Q risk score should patients be offered a statin?

A

10% and above

188
Q

What is the first line treatment for sinus bradycardia presenting with features of heart failure?

A

500 micrograns IV atropine

Transvenous pacing if this fails or risk of asystole

189
Q

Which features of a bradycardia suggest potential risk of asystole?

A

Complete heart block with broad complex QRS
Recent asystole
Mobitz type II AV block
Ventricular pause >3 seconds

190
Q

What ecg changes are associated with tricyclic overdose?

A

Prolongation of PR and QT interval
Broad QRS
Conduction delay
Ventricular tachycardia

191
Q

What is the management for acute right ventricular failure?

A

Fluid resuscitation carefully titrated to left atrial pressure to maintain enough pressure for peripheral perfusion but without excess left atrial filling which would lead to pulmonary oedema
Use Swan Ganz catheter to monitor pulmonary capillary wedge pressure as a surrogate for left atrial pressure

192
Q

What is a strain pattern on ECG?

A

Large voltages in chest leads

ST depression and T wave inversion

193
Q

Which bugs commonly cause bacterial endocarditis?

A

Streptococcus viridans
Staph aureus
Staph epidermidis

194
Q

What are the antibiotics of choice for endocarditis?

A

Native valve: amoxicillin, gent
Native valve with sepsis/penicillin allergy or MRSA: vancomycin and gent
Native with sepsis and risks for gram neg: vancomycin, meropenem
Prosthetic valve: vancomycin, gent and rifampicin

195
Q

For how long post MI can a patient not drive for?

A

4 weeks

196
Q

What signs might you find in infective endocarditis?

A 
Clubbing 
Murmur 
Splinter haemorrhages 
Roth spots 
Oslers nodes
Janeway lesions 
Splenomegaly
197
Q

Which drugs have been shown to reduce mortality in patients with chronic heart failure?

A

ACE inhibitors
Spironolactone
Beta blockers
Hydralazine with nitrates

198
Q

Which drugs are first line in heart failure?

A

ACE inhibitor and beta blocker

199
Q

What is second line therapy for heart failure?

A

Aldosterone antagonist, ARB or hydralazine with a nitrate

200
Q

What should be tried if first and second line therapies fail in cardiac failure?

A

Cardiac resychronisation therapy
Digoxin
Ivabradine: if heart rate >75 and left ventricular fraction <35%

201
Q

What are 5 poor prognostic markers which are predictive of sudden cardiac death in hypertrophic cardiomyopathy?

A

Syncope
Family history of HOCM and sudden cardiac death
Maximum left ventricular thickness greater than 3cm
Blood pressure drop during peak exercise on stress testing
Documented runs of non sustained VT on 24 hour tape

202
Q

What is a cardiac index?

A

Parameter that relates cardiac output to body surface area

203
Q

What is a cardiac myxoma? How does it present?

A

Benign primary cardiac tumour

May present as heart failure, syncope, embolisation, fever, weight loss, arthralgia, raynauds

204
Q

Which drug should be administered to normalise clotting prior to decannulation and chest closure in a coronary artery bypass procedure?

A

Protamine sulphate to reverse large doses of heparin given through the procedure

205
Q

What is the difference between class I a b and c anti arrhythmogenic drugs?

A

All block sodium channels

1a: increase AP duration
1b: decrease AP duration
1c: no effect on AP duration

206
Q

What signs would you expect to find in a patient with mitral stenosis?

A 
Low volume pulse
Irregularly irregular pulse
Mitral facies 
Mid diastolic murmur
Opening snap
Tapping apex beat
207
Q

What type of pulse is associated with heart failure?

A

Pulsus alternans - pulse waves of differing amplitudes and/or intensity

208
Q

If a patient has had an MI, how long before they are recommended to fly?

A

7-10 days if successfully treated

209
Q

Why might a patient with turners syndrome have aortic stenosis?

A

Bicuspid aortic valve

210
Q

What is brugada syndrome?

A

Genetic condition, mutation in cardiac sodium channel gene that causes arrhythmia and high risk of sudden death
Brugada sign on ECG: coved ST elevation >2mm in >1 of V1-V3 followed by negative t wave
Saddleback shaped ST elevation

211
Q

What are features of pericarditis?

A 
Chest pain: may be pleuritic, relieved by sitting forwards
Non productive cough
Dyspnoea
Flu like symptoms
Pericardial rub
Tachypnoea
Tachycardia
212
Q

What are causes of pericarditis?

A 
Viral infections: coxsackie 
Tuberculosis
Uraemia
Trauma
Post MI, Dressler's syndrome
Connective tissue disease
Hypothyroidism
213
Q

What are ECG changes associated with pericarditis?

A

Widespread saddle shaped ST elevation

PR depression

214
Q

What are the major duckett jones criteria for rheumatic fever?

A 
Polyarthritis
Erythema marginatum 
Rheumatoid nodules 
Cardiac involvement 
Sydenham's chorea
215
Q

What are first line drugs for angina?

A

All patients should receive aspirin and statin in absence of contraindication
Sublingual GTN
Beta blocker or calcium channel blocker first line
If calcium channel blocker as monotherapy: rate limiting like verapamil or diltiazem
If combo with beta blocker: long acting like nifedipine

216
Q

Which drug should be added in when angina is not adequately controlled with beta blocker monotherapy?

A

Nifedipine

217
Q

What are features of complete heart block?

A 
Syncope
Heart failure
Regular bradycardia
Wide pulse pressure
JVP cannon waves 
Variable intensity of S1
218
Q

What is corrigans sign?

A

Abrupt distension and collapse of carotid arteries as a sign of aortic regurgitation

219
Q

What signs are associated with aortic regurgitation?

A

Corrigans: vigorous arterial pulsations in neck
De mussets sign: head nodding with each pulse
Quinckes: capillary pulsation in nail beds
Duroziezs sign: diastolic murmur when femoral artery compressed and auscultated proximally
Austin flint: functional mid diastolic murmur - regurgitant jet interferes with opening of anterior mitral valve leaflet

220
Q

What is cavallos sign?

A

Tricuspid regurgitation is louder with inspiration

221
Q

What is the most common cause of death following an MI?

A

Cardiac arrest - VF

222
Q

What are some complications of an MI?

A 
Cardiac arrest
Cardiogenic shock
Chronic heart failure
Tachyarrhythmia
Bradyarrhythmia 
Pericarditis 
Left ventricular aneurysm
Left ventricular free wall rupture
VSD
Acute mitral regurg
223
Q

How does a ventricular aneurysm post MI present?

A

Persistent ST elevation and left ventricular failure

Can present with stroke if thrombus forms

224
Q

How would a patient with a left ventricular free wall rupture post MI present?

A

Acute heart failure secondary to tamponade - raised JVP, pulsus paradoxus, diminished heart sounds

225
Q

How is heart failure diagnosed?

A

If patient had previous MI: echo within 2 weeks

If no MI: serum BNP, if levels high- echo in 2 weeks. If levels raised- echo in 6 weeks

226
Q

Which bug is most likely to cause bacterial endocarditis in patients with previously abnormal valves?

A

Streptococcus viridans

227
Q

What ecg findings are suggestive of MI?

A

ST elevation of 1mm in limb leads
ST elevation 2mm chest leads
New LBBB

228
Q

What ecg changes are associated with hypokalaemia?

A

ST depression
U waves
Inverted t waves
Prolonged PR interval

229
Q

How do you decide how to treat a patient with angina sounding chest pain?

A 
NICE angina table 
Risk assess to determine who to treat 
If risk is over 90% - treat
If 61-90 arrange coronary angiography 
If 30-60 non invasive functional imaging
If 10-29 CT calcium scoring 
If less than 10%, not cardiac
230
Q

What is angina decubitus?

A

Chest pain provoked by lying flat

231
Q

What immediate management should be given for AF precipitating LVF?

A 
Diuretics
ACE inhibitors
Nitrates
Digoxin
Oxygen
Diamorphine
232
Q

What are major risk factors for the development of ischaemic heart disease?

A 
Obesity
Diabetes Mellitus 
Tobacco Use 
Latent Life Style (lack of exercise, Stress)
Hypertension
Hypercholesterolemia
Age
233
Q

What lifestyle changes should be used to manage ischaemic heart disease?

A

Exercise Preventive treatment
Diet: Low fat, low cholesterol diet
Cessation of smoking
Red wine (in moderation)

234
Q

What are management options for hypercholesterolaemia? What are the mechanisms of action of these drugs?

A

Statins: HMG CoA reductase inhibitor
Ezetimibe: reduces cholesterol absorption in small intestine
PCSK09 Inhibitors: Evolocumab, Alirocumab, increase LDL receptor numbers on surface of hepatocytes
Fibrates: increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III
Nicotinic acid: inhibits hepatocyte diacylglycerol acyltransferase–2, a key enzyme for TG synthesis
Colestipol: bile acid sequesterant

235
Q

What are the options for smoking cessation medications?

A

Nicotine replacements: Gum, patches, inhaler, nasal spray, tablets/lozenges
Bupropion 100 mg OD – 450 mg /day
Varenicline 0.5mg OD – 1 mg BD

236
Q

What drugs can be used to manage ischaemic heart disease?

A

Beta Blockers: bisoprolol
Calcium Channel Blocker: diltiazem
Nitrates: Isosorbide mononitrate (tablet form) 50-60mg/day
Antiplatelet Medication: Aspirin, Clopidogrel , prasugrel, ticagrelor

237
Q

What should be done in the acute management of unstable angina?

A 
Heparin: Clexane, Fondaparinux
IIb-IIIa blockers– Abciximab, Tirofiban, Eptifibatide
Thrombolytics
Angioplasty
CABG
238
Q

What is wellens syndrome?

A

Critical proximal LAD coronary artery stenosis in patients with unstable angina

239
Q

What are common causes of heart failure?

A 
Ischemic heart Disease
Diabetes
Hypertension
Valvular Heart Disease
ETOH Abuse
Obesity
Cigarette Smoking
Hyperlipidemia
Physical Inactivity
Sleep Apnea
240
Q

What are some less common causes of heart failure?

A 
Familial Hypertrophic CM
Postpartum CM
Thyroid Abnormality
Connective Tissue Disorders
Toxin Exposure
Myocarditis
Sarcoidosis
Hemochromatosis
Medication Exposure
241
Q

What is the New York heart association functional classification of heart failure?

A

Class I: No abnormal symptoms with activity
Class II: Symptoms with normal activity
Class III: Marked limitation due to symptoms with less than ordinary activity
Class IV: Symptoms at rest and severe limitations in functional activity

242
Q

What are the conservative treatment options for heart failure?

A 
Diet: Salt restriction, Fluid restriction, Weight  loss, Lipid control, Cachexia
Alcohol
Smoking
Exercise
Immunization
Cardiac Rehab
Palliative Services
Social Support
243
Q

Which drugs are used in the management of heart failure?

A 
ACE-Inhibitors / angiotensin receptor blockers
Beta Blockers
Spironolactone
Diuretics
Digoxin
244
Q

What is the indication and goal in using ace inhibitors in heart failure?

A

Indication: All HF patients with systolic Dysfunction (symptomatic or not)
Goal: Reduce morbidity and Mortality

245
Q

What precautions should be taken when using ace inhibitors in the management of heart failure?

A

Baseline Serum K+ and Cr. at initiation of therapy required

Careful monitoring if sBP <100mmHg, or if elevated serum Cr.

246
Q

What is the indication and goal in using beta blockers in heart failure?

A

Indication: All HF patients with Systolic Dysfunction except those with symptoms at rest
Goal: Improve morbidity and mortality. 34% decrease in mortality

247
Q

What precautions should be taken when using beta blockers in heart failure?

A

Monitor for drop in BP or worsening dyspnoea
Reduce / Hold diuretics if serum Cr increase by over 30% from baseline
Caution in patients with COPD, Asthma, may precipitate bronchospasm

248
Q

What is the indication for using spironolactone in heart failure?

A

Symptom at rest or new onset of symptom in last 6mo

Beneficial for moderateto severe HF (Class III)

249
Q

What precautions should be taken when using spironolactone in heart failure?

A

Monitor kidney function and Potassium

Max 50 mg/day

250
Q

What is the indication for using digoxin in heart failure?

A

HF and Atrial fibrillation

Patients still symptomatic despite use of Diuretics, ACEI and b-Blockers

251
Q

What dose of digoxin is used in heart failure?

A

0.125 – 0.25mg /d (lower than for control of AF)

252
Q

What precautions should be taken when using digoxin for heart failure?

A

Digoxin levels [when toxicity is suspected]
Pushed to back burner b/c of recent discovery that it can increases risk of death from any cause amongst women [not men] w/HF and decreased LVEF

253
Q

What are management options for heart failure with AF?

A

Rate control: Digoxin, Betablockers
Rhythm management: Amiodarone, Cardioversion
Reduce risk: warfarin
Control of symptoms: Furosemide, IV GTN
Managing the underlying process: ACE inhibitors, Betablockers, Spironolactone, entresto, Statins

254
Q

Which drugs are contraindicated in heart failure?

A

Calcium channel antagonists – except for amlodipine
Positive inotropes
Antiarrhythmics – except for amiodarone and digoxin
Alpha blockers
NSAIDs

255
Q

What interventional options are available to manage heart failure?

A

Rhythm control: Drugs, Pacemakers, ICD, Cardiac resynchronisation therapy pacemaker or defibrillator
Structural alterations: Valve repair, CABG, LV remodelling, left ventricular assist device, Heart transplantation

256
Q

What is the mechanism of action of class 1a anti arrhythmic drugs?

A

Blocker’s of fast Na+ channels
Cause moderate Phase 0 depression
Prolong repolarization
Increased duration of action potential

257
Q

What is the standard antiarrhythmic for paroxysmal VT?

A

Amiodarone

258
Q

Give some examples of class 1A antiarrhythmic drugs

A

Quinidine: treat atrial and ventricular arrhythmias, increases refractory period
Procainamide: increases refractory period but side effects
Disopyramide: extended duration of action, used only for treating ventricular arrhythmias

259
Q

What is the mechanism of action of class 1B antiarrhythmic drugs?

A

Blocker’s of fast Na+ channels
Weak Phase 0 depression
Shortened depolarization
Decreased action potential duration

260
Q

What are some examples of class 1B antiarrhythmic drugs?

A

Lidocane
Lidocaine: blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmias
Mexiletine: oral lidocaine derivative, similar activity
Phenytoin: anticonvulsant that also works as antiarrhythmic similar to lidocane

261
Q

What is the mechanism of action of class 1C antiarrhythmic drugs?

A

Block fast Na+ channels
Strong Phase 0 depression
No effect of depolarization
No effect on action potential duration

262
Q

What are some examples of class 1C antiarrhythmic drugs?

A

Flecainide: Slows conduction in all parts of heart, inhibits abnormal automaticity
Propafenone: slows conduction, Weak beta blocker, Also some Ca2+ channel blockade

263
Q

What is the mechanism of action of class II antiarrhythmic drugs?

A

Blockade of myocardial beta adrenergic receptors

Direct membrane stabilising effects related to Na+ channel blockade

264
Q

What are some examples of class II antiarrhythmic drugs?

A

Propranolol: myocardial beta–adrenergic blockade and membrane-stabilising effects, Slows SA node and ectopic pacemaking, Can block arrhythmias induced by exercise or apprehension
Other beta–adrenergic blockers have similar therapeutic effect: Metoprolol, Nadolol, Atenolol, Pindolol, Stalol, Timolol, Esmolol

265
Q

What is the mechanism of action of class III antiarrhythmic drugs?

A

K channel blockers

Cause delay in repolarization and prolonged refractory period

266
Q

What are some examples of class III antiarrhythmic drugs?

A

Amiodarone: prolongs action potential by delaying K+ efflux but
many other effects characteristic of other classes
Ibutilide: slows inward movement of Na+ in addition to delaying K + influx
Bretylium: first developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial
infarction
Dofetilide: prolongs action potential by delaying K+ efflux with no
other effects

267
Q

What can be a problem with using Amiodarone as an antiarrhythmic?

A

Takes a long time to get to therapeutic levels and then long to get out of the system after

268
Q

What is the mechanism of action of class IV antiarrhythmic drugs?

A

Ca2+ channel blockers

slow rate of AV-conduction in patients with atrial fibrillation

269
Q

What are examples of class IV antiarrhythmic drugs?

A

Verapamil: blocks Na+ channels in addition to Ca2+, also slows SA node in tachycardia
Diltiazem

270
Q

What is one of biggest problems faced when using antiarrhythmic drugs?

A

Antiarrhythmics can cause arrhythmia
Example: Treatment of a non-life threatening tachycardia may cause fatal ventricular arrhythmia
Must be vigilant in determining dosing, blood levels, and in follow-up when prescribing antiarrhythmics

271
Q

What are the criteria for starting antihypertensive drug treatment?

A

Offer antihypertensive drug treatment to people aged under 80 years with stage 1 hypertension who have one or more of the following:
target organ damage
established cardiovascular disease
renal disease
diabetes
10-year cardiovascular risk equivalent to 20% or greater
Offer antihypertensive drug treatment to people of any age with stage 2 hypertension

272
Q

What should be done to manage resistant HTN?

A

Consider further diuretic therapy with low-dose spironolactone (25 mg once daily) if the blood potassium level is 4.5 mmol/l or lower
Consider higher dose thiazide like diuretic treatment if the blood potassium level is higher than 4.5 mmol/l consider an alpha or beta-blocker
Seek expert advice if it has not yet been obtained

273
Q

What is a stokes Adams attack?

A

Collapse without warning associated with loss of consciousness for a few seconds
Typically complete heart block is seen on ecg during attack

274
Q

What is the mechanism of the NOACs?

A

Direct thrombin inhibitor: Dabigatran

Direct factor Xa inhibitor: Rivaroxaban, Apixaban, Edoxaban

275
Q

What is heydes syndrome?

A

Aortic stenosis and colonic angio dysplasia

276
Q

Which patients with stage 1 HTN need treatment?

A 
If <80 and any of:
Target organ damage
Established CV disease
Renal disease
Diabetes
10 year CV risk 20% or more
277
Q

What lifestyle advice should be offered for HTN patients?

A

Low salt: less than 6g/day, ideally 3g/day
Reduce caffeine intake
Smoking cessation
Reduce alcohol consumption
Balanced diet with plenty of fruit and vegetables
Exercise more
Lose weight

278
Q

What are ecg features of Wolff Parkinson white syndrome?

A

Short PR interval
Wide QRS with slurred upstroke (delta wave)
LAD if right sided accessory pathway
RAD if left sided accessory pathway

279
Q

Which patients with NSTEMI should be given IV glycoprotein IIb/IIIa receptor antagonists such as eptifibatide or tirofiban?

A

Intermediate or higher risk of adverse cardiovascular events (6 month mortality above 3% GRACE score) and who are scheduled to undergo angiography within 96 hours of hospital admission

280
Q

What are classification systems for dissecting aortic aneurysms?

A

De Bakey

Standford

281
Q

How is a diagnosis of heart failure made?

A

If previous MI: echo within 2 weeks

If no previous MI: BNP, if levels high echo within 2 weeks, if levels raised echo within 6 weeks

282
Q

What is bifascicular block?

A

Combination of RBBB with left anterior or posterior hemiblock
Eg RBBB with LAD

283
Q

What is trifascicular block?

A

Features of bifascicular block: RBBB, LAD plus 1st degree heart block

284
Q

What 4 different methods can be used to reduce blood pressure?

A

Heart - Reduce CO - SV + HR, ie Betablocker
Arteries - Reduce PVR - Vasodilate
Kidney - Remove fluid - input decrease, or inc output (Diuretics)
Brain - tell CVS/RAS reduce BP

285
Q

What electrolyte changes do thiazide diuretics cause?

A 
K decrease
Na decease
Glucose increase 
Cholesterol increase
Urate increase
286
Q

What are the different potassium sparing diuretics?

A

Aldosterone antagonist: Spironolactone 25 mg OD, Eplerenone

Epithelial Na+ channel blocker: Amiloride 5 mg OD, Triamterene

287
Q

What are side effects of loop diuretics?

A

Na loss
K/H loss, leading to hypokalaemic alkalosis
Hypocalcaemia, use as treatment for hypercalcaemia
Rashes esp bullous
Ototoxicity
Can worsen digoxin toxicity (via hypokalaemia)

288
Q

What are side effects of beta blockers?

A 
Lethargy
Heart failure
Bronchospasm
PVD
Raynaud’s
Bad dreams
Explosive diarrhoea
Reduced HDL-cholesterol
289
Q

What are side effects of verapamil?

A

Heart failure/Heart block
Peripheral oedema
Facial flushing
Headaches

290
Q

What are side effects of calcium channel blockers?

A

Marked facial flushing
Headaches
Peripheral oedema
Polyuria (exacerbate prostatism)

291
Q

What are side effects of ACE inhibitors?

A

Caution in CKD, esp renal artery stenosis (or possibility)
Hyperkalaemia
STOP in above, AKI, pre-op, angiogram, sepsis
Cough, Angio-oedema

292
Q

What is the target for salt intake to control blood pressure?

A

<6g per day

293
Q

What is hypertensive urgency?

A

Defined as ‘DBP >120 mm Hg in absence of acute or rapidly worsening target organ damage’
Not nec admit (daily OP review possible)

294
Q

What is HTN emergency?

A

Accelerated/Malignant
Defined as ‘acute or rapidly worsening target organ damage
occurring in a hypertensive pt in assoc with BP’, but irrespective of specific BP level attained (eg 140/90 in Pre/Eclampsia)
Target organs = CCF, dissection, AKI, encephalopathy, retinopathy

295
Q

What are different grades of murmur?

A

1 - heard by expert in optimum conditions
2- non expert in optimum conditions
3- easily heard, no thrill
4-loud murmur, palpable thrill
5- very loud, heard over wide area, palpable thrill
6- extremely loud heard without stethoscope

296
Q

What does a VSD sound like?

A

Harsh pansystolic murmur heard at left lower sternal edge

May have a thrill

297
Q

What does an ASD sound like?

A

Soft ejection systolic at left upper sternal edge

May be wide, fixed splitting of S2

298
Q

What does pulmonary stenosis sound like?

A

Ejection systolic murmur at left upper sternal edge
Radiation to back
Ejection click

299
Q

Which gene mutations can cause familial hypercholesterolaemia?

A

LDLR mutations
ApoB mutations
PCSK9

300
Q

How does LDL cholesterol cause atherosclerosis?

A 
High plasma LDL
LDL infiltration into intima 
Macrophages and oxidative metabolism leads to 
Foam cells
Fatty streak
Endothelial injury
Adherence of platelets 
Release of PDGF 
Advanced calcific lesion
301
Q

What are therapeutic options for lowering LDL cholesterol?

A

HMG-CoA reductase inhibitors: Atorvastatin, Fluvastatin, Lovastatin, Pravastatin, Rosuvastatin, Simvastatin
Bile acid sequestrants: Cholestyramine, Colesevelam, Colestipol
Cholesterol absorption inhibitor: Ezetimibe
Nicotinic acid: Niacin
Dietary Adjuncts: Soluble fiber, Soy protein, Stanol esters

302
Q

What is the mechanism of action of bile acid sequestrants in lowering cholesterol?

A

Bind bile acids in GI tract

Disrupt enterohepatic circulation of bile acids by preventing reabsorption

303
Q

What is the mechanism of action of statins?

A

HMG co A reductase inhibitor
Reduction in hepatic cholesterol synthesis lowers intracellular cholesterol, which stimulates upregulation of the LDL receptor and increases uptake of non-HDL particles from systemic circulation

304
Q

What are risk factors for the development of myopathy when using statins?

A 
Concomitant Use of Meds: Fibrate, Nicotinic acid, Cyclosporine
Antifungal azoles, Macrolide antibiotics, HIV protease inhibitors, Verapamil, Amiodarone
Advanced age (especially >80 years)
Women > Men especially at older age
Small body frame, frailty
Multisystem disease
Multiple medications
Perioperative period
Alcohol abuse
Grapefruit juice
305
Q

Who needs statins as primary prevention? What dose?

A

Diabetes, CVD risk greater than 20% over 10 years
Atorvastatin 20mg od
Type 1 >40 years or duration 10years

306
Q

Who needs statins for secondary prevention? What dose?

A

All CVD: CHD, Stroke, PVD, TIA

Atorvastatin 80mg od

307
Q

What is the mechanism of action of ezetimibe?

A

Inhibits absorption of cholesterol from small intestine by blocking NPC1L1 (niemann pick C1 like 1) protein on epithelial cells

308
Q

What is the mechanism of action of fibrates?

A

Agonists of the PPAR-alpha receptor in muscle, liver, and other tissue results in:
Decreased hepatic triglyceride secretion, Increased lipoprotein lipase activity, and thus increased VLDL clearance, Increased HDL, Increased clearance of remnant particles

309
Q

What are indications for fibrates?

A

Hypercholesterolaemia, hypertriglyceridaemia, low HDL

310
Q

What are side effects of fibrates?

A

myalgia, gallstones, nausea

311
Q

What is the mechanism of action of nicotinic acid to reduce cholesterol?

A

Decreased hepatic production of VLDL and uptake of apolipoprotein A-1 results in reduced LDL-C levels and increased HDL-C levels

312
Q

What are side effects of nicotinic acid?

A

flushing, headaches, poorer glycaemic control

313
Q

What are nice guidelines on fibrates use?

A

Indicated for treatment of hypertriglyceridaemia
Assess for secondary causes: hyperglycaemia, hypothyroidism, renal impairment, liver disease, alcohol
Agent of choice = fenofibrate
Treat if TG > 4.5 even if not on a statin
If on a statin, add a fibrate if TG > 2.3

314
Q

What is PCSK9? What role does this have in controlling LDL levels?

A

Pro protein convertase subtilisin like Kexin type 9
Secreted protease which is removed via LDL receptor
LDL receptor numbers on surface decrease and so plasma LDL rises

315
Q

What is the Framingham diagnostic criteria for heart failure?

A

Major: acute pulmonary oedema, cardiomegaly, hepatojugular reflux, neck vein distension, PND or orthopnoea, rales, third heart sound gallop
Minor: ankle oedema, dyspnoea on exertion, hepatomegaly, nocturnal cough, pleural effusion, tachycardia >120
Heart failure if 2 major or 1 major 2 minor criteria

316
Q

What is the Stanford classification?

A

Aortic aneurysms
Type A: ascending aorta and arch
Type B: begins beyond brachiocephalic vessels

317
Q

What is the deBakey classification?

A

Aortic aneurysms
DeBakey 1: originates in ascending aorta, to arch
2: ascending aorta
3: distal aorta

318
Q

What is hammans sign?

A

In mediastinal emphysema, crunching sound over precordium as a result of heart beating against air filled tissues

319
Q

What is Levines sign?

A

Use of clenched fist by patients who are describing nature of pain in ACS

320
Q

What is olivers sign?

A

Tracheal tug in aortic aneurysm

Cricoid cartilage is pushed upward so downward pull on trachea with each heartbeat

321
Q

What is cardarellis sign?

A

Pulsation felt in trachea due enlarged aortic aneurysm

322
Q

What are giant A waves?

A

Feature of JVP when poorly compliant right ventricle or tricuspid stenosis, increasing impedance against which right atrium has to eject blood

323
Q

What happens to JVP in constrictive pericarditis?

A

JVP high with abrupt fall in systole - x decent

May rise with inspiration - kussmauls sign

324
Q

What is appropriate treatment for a patient with AF and heart failure?

A

Digoxin and furosemide

325
Q

What is a reassuring feature of ectopic heart beats?

A

If they disappear with exercise

326
Q

What is the management for a patient with long QT interval and family history of sudden death?

A

Implantable defibrillator

327
Q

What 2 syndromes cause congenital long QT syndrome?

A

Romano Ward syndrome: autosomal dominant, QT prolongation, ventricular tachyarrhythmia
Jervell and Lang-Nielsen syndrome: autosomal recessive, deafness, QT prolongation, ventricular arrhythmia

328
Q

Which type of arrhythmia are patients with long QT syndrome predisposed to?

A

Polymorphic ventricular tachycardia

329
Q

Why do patients with Marfans get aortic dissection?

A

Marfans causes dilation of aortic sinuses causing dilated aortic root which can lead to rupture or dissection

330
Q

What do large congenital VSDs cause?

A

Volume overload in left ventricle causing displaced apex and can lead to left ventricular failure (blood pumped through VSD goes through lungs and back around again, having to work harder)
Pulmonary HTN causing loud P2 and hepatomegaly because of right sided congestion (left to right shunt means pulmonary vasculature fails to mature normally and so remains thick walled and muscular)
Turbulent flow across septum causing pansystolic murmur at left sternal edge
Left untreated, eisenmengers syndrome as shunt reverses due to high pulmonary pressures - cyanotic and hypoxic

331
Q

Who should be offered anti hypertensive medication?

A 
Aged less than 80 with stage 1 HTN (ambulatory 135/85 or less) with one or more of: 
Target organ damage 
Established CV disease
Renal disease
Diabetes
10 year CV risk of 20% or more 
Stage 2 HTN diagnosis
332
Q

How should a heart failure be investigated?

A

Previous MI: echo within 2 weeks

No previous MI: measure BNP, if high (>400) echo in 2 weeks, if raised (100-400) echo in 6 weeks

333
Q

What is the management of angina pectoris?

A

Lifestyle changes
Aspirin
Statin
Sublingual GTN for acute attacks
Beta blocker or calcium channel blocker first line
If Ca blocker monotherpy - verapamil or diltiazem
If combotherapy - nifedipine
If poor response, add other drug
Other drugs to be considered: long acting nitrate, ivabridine, nicorandil, ranolazine
Only add 3rd drug while waiting for PCI/CABG assessment

334
Q

What are secondary causes of HTN?

A 
Renovascular: fibromuscular dysplasia, renal artery stenosis
ADPKD
CKD
Pheochromocytoma
Conns syndrome 
Hyperparathyroidism 
Acromegaly
Hyperthyroidism 
Hypothyroidism 
Congenital adrenal hyperplasia 
Cushing's syndrome 
OSA
335
Q

When is surgical correction of an ASD recommended?

A

Before onset of pulmonary HTN

336
Q

When is ligation of a patent ductus arteriosus advised?

A

If defect has not corrected spontaneously after 6 months

Immediately in neonates with heart failure not responding to medical management

337
Q

When should correction of tetralogy of fallot be done?

A

At 1-5 years of age

Palliative shunting can be done prior to this

338
Q

When do VSDs require surgical correction?

A

Large haemodynamically significant perimembranous ventricular septal defects may need closure in first year

339
Q

What should target blood pressure be for diabetics?

A

If end organ damage: <130/80

Otherwise: <140/80

340
Q

What are principle signs of cor pulmonale?

A

Raised JVP
Third heart sound causing gallop rhythm
Ankle oedema

341
Q

What are some causes of aortic regurgitation?

A 
Rheumatic heart disease 
Congenital bicuspid aortic valve
HTN
Marfans (dilated aortic root)
Subacute bacterial endocarditis 
Syphilitic aortitis 
Degenerative valve disease
SLE 
Ankylosing spondylitis 
Takayasus disease
342
Q

What is the antiplatelet guidance after MI?

A

NSTEMI: aspirin lifelong, clopidogrel or ticagrelor 12 months
STEMI: aspirin lifelong, clopidogrel or ticagrelor 1m if no stent, 12m if drug eluting stent

343
Q

What are investigations for primary hyperaldosteronism?

A 
U and Es: hypokalaemia 
High serum aldosterone
Low serum renin
High resolution CT abdo
Adrenal vein sampling
344
Q

What is the management of primary hyperaldosteronism?

A

Adrenal adenoma: surgery

Bilateral adrenocortical hyperplasia: aldosterone antagonist - spironolactone

345
Q

Which diuretics are now recommended by nice for use in HTN?

A

Chlorthalidone

Indapamide

346
Q

What are step 4 management options for HTN?

A

If potassium <4.5, add spironolactone
If potassium >4.5 add higher dose thiazide like diuretic
If further diuretic not tolerated/contraindicated/ ineffective, consider alpha or beta blocker

347
Q

What is the Simon Broome criteria for diagnosis of familial hypercholesterolaemia?

A

Total cholesterol >7.5 and LDL-C >4.9
For definite: tendon xanthoma in patient or 1st/2nd degree relative or DNA evidence of FH
For possible: family hx MI below age 50 in 2nd degree relative, age 60 in 1st degree or family hx of raised cholesterol

348
Q

What is the management of familial hypercholesterolaemia?

A

Referral to specialist lipid clinic
Max dose statin
First degree relative offered screening including children by age 10
Statin discontinued in women 3 months before conception due to risk of congenital defects

349
Q

What ECG changes are an indication for thrombolysis or percutaneous intervention?

A

ST elevation of >2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) or
ST elevation greater than 1mm in greater than 2 consecutive inferior leads (II, III, avF, avL) or
New left bundle branch block

350
Q

Why might a patient develop mitral regurgitation post MI?

A

Inferior wall dysfunction, disruption of posteromedial papillary muscle

351
Q

What is a grace score?

A

Estimates 6 month mortality for patients with acs

Age, HR, BP, creatinine, arrest?, ST changes, cardiac enzymes, signs of CHF

352
Q

How is symptomatic bradycardia treated?

A

IV atropine

353
Q

What are adverse features of bradycardia?

A

Shock
MI
Heart failure
Syncope

354
Q

What is an important contraindication to NOAC for anticoagulation of AF?

A

Valvular disease

355
Q

What is wellens syndrome?

A

electrocardiographic manifestation of critical proximal left anterior descending coronary artery stenosis in patients with unstable angina. It is characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads

356
Q

What are signs of compromise in arrhythmia?

A

Shock
Chest pain
Syncope
Heart failure

357
Q

How is angina confirmed diagnostically?

A

2ww chest pain clinic
No Hx heart disease: CT coronary angio, CT calcium scoring
Hx IHD: stress imaging (echo, MRI, or myocardial perfusion imaging)

358
Q

What are features of trifascicular block on ecg?

A

First degree heart block
Left axis deviation
Right bundle branch block

359
Q

What are X-ray findings of heart failure?

A 
Alveolar oedema (bats wings)
Kerley b lines (interstitial oedema)
Cardiomegaly
Dilated prominent upper lobe vessels 
Effusion
360
Q

What are causes of right bundle branch block?

A 
Normal variant with age
Right ventricular hypertrophy
Chronic increased right ventricle pressure (cor pulmonale) 
Pulmonary embolism
Myocardial infarction
ASD
Cardiomyopathy or myocarditis
361
Q

What are third and fourth heart sounds?

A

S3: diastolic filling of ventricle, heard in left ventricular failure, constrictive pericarditis, mitral regurgitation
S4: atrial contraction against stiff ventricle, heard in aortic stenosis, HOCM, HTN

362
Q

What is the most common cause of endocarditis following prosthetic valve surgery?

A

Staphylococcus epidermidis

363
Q

What are indications for surgery in aortic stenosis?

A

Symptomatic
CCF
Mean pressure gradient >40
Concomitant CABG requirement

364
Q

What are signs of severity in aortic stenosis?

A 
Narrow pulse pressure 
Slow rising pulse
Delayed closure of A2 or reversed splitting of 2nd heart sound
Heaving apex beat
Features of HF
Symptomatic
365
Q

What are differentials for a patient with a sternotomy scar but no murmur or scars on the legs?

A

Tissue valve replacement
CABG using internal thoracic vein
Repair of congenital cardiac disease

366
Q

What are INR targets for valve replacements?

A

Bioprosthetic: aortic no warfarin, mitral 2.5 for 3 months
Metallic: aortic 3, mitral 3.5, lifelong warfarin

367
Q

What are indications for CABG?

A

Left main stem disease
2 or more vessel disease
Failure of medical management
Concomitant aortic valvular replacement

368
Q

Which vessels can be used for CABG?

A 
Great saphenous
Internal thoracic (mammary) vein
369
Q

What medications are required post CABG?

A

Dual antiplatelet for 12 months, then aspirin alone
Cardio selective beta blocker (bisoprolol)
ACE inhibitor or ARB

370
Q

What are causes of mitral regurgitation?

A

Chronic: myxomatous degeneration, functional (with LV dilatation)
Acute: infective endocarditis, papillary muscle rupture (Inf or post MI)

371
Q

What are signs of severity in mitral regurgitation?

A

Displaced or thrusting apex beat

Left ventricular failure

372
Q

What are causes of RVF?

A

Acute: MI, PE, infective endocarditis
Chronic: LVF, cor pulmonale

373
Q

What are causes of LVF?

A

Acute: MI, infective endocarditis
Chronic: ischaemic cardiomyopathy, HTN cardiomyopathy, valvular heart disease

374
Q

What are ecg criteria for left ventricular hypertrophy?

A

R wave greater than 25mm in V5/6

Or R plus S greater than 35mm

375
Q

What are signs of cor pulmonale on ECG?

A

RAD
P pulmonale
Dominant R wave in V1
Inverted T waves in chest leads

376
Q

What are signs of cor pulmonale on a chest X-ray?

A

Dilatation right atrium
Enlarged right ventricle
Prominent pulmonary arteries

377
Q

In which condition are Roth spots seen in the retina?

A

Bacterial endocarditis

378
Q

What is the duke criteria for endocarditis?

A

Major: 2 positive blood cultures for organism known to cause IE, echo evidence
Minor: cardiac lesion or IVDU, fever >38, vascular phenomenon, immunological phenomenon, blood culture, echo

Phase 3 (23 decks)

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