Cardiology Flashcards

1
Q

Who is eligable for AAA screening?

A

Ultrasound offered to men over 65

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2
Q

What is the differential for aortic stenosis?

A

HCM- gets louder on Valsalva (more preload- whereas AS gets quieter) and HCM gets quieter with squatting (afterload)

VSD
Aortic sclerosis- normal pulse (not slow rising) doesn’t radiate to carotids
Aortic flow

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3
Q

Which bacteria is responsible for rheumatic fever?

A

Streptococcus pyogenes

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4
Q

Name two conditions associated with aortic stenosis

A

Angiodysplasia (cause of GI bleeds in the elderly)

Coarctation with bicuspid aortic valve (check BP + radioradial delay)

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5
Q

On examination you have detected an ejection systolic murmur, what further investigations would you like to do:

A

ECG- looking for LVH voltage criteria
(S wave depth in V1 + R wave height in V5 or V6 >35mm)
CXR: calcified aortic valve
Echocardiogram (severe is LVOT gradient >50mmHg and valve area less than 1cm3 area)

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6
Q

Three main symptoms of aortic stenosis:

A
  1. Chest pain
  2. Exertional dyspnoea
  3. Syncope
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7
Q

What is P mitrale and the causes?

A

A bifid P wave

In isolation- mitral stenosis and volume overload slowing emptying
With LVH- hypertension, aortic stenosis, HCM

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8
Q

What is the Duke’s criteria:

A

2M; or 1M + 2m; or 5m

M:
2 +ve blood cultures (or persistently +ve when taken at varied times)
Echo- abscess, dihiscence, vegetation, new regurgitation

m:
Atypical organism on blood cultures; suggestive echo; pyrexia; embolic phenomena; high CRP or ESR; prosthetic valve/IVDU

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9
Q

Common causes of infective endocarditis:

A
Staph aureus (commonest)
Strep viridians

Staph epidermidis; enterococci; diptherioids; HACEK (G -ve)

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

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10
Q

If someone with infective endocarditis has an abscess at their aortic root, what ECG signs may be present?

A

PR prolongation > complete AV block

The AV node in the right atrium is closely approximated to the aortic root

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11
Q

Causes of Aortic Regurgitation:

A

Valvular:
Acute- endocarditis (no collapsing pulse)
Chronic- rheumatic fever, rheumatoid arthritis

Aortic root
Acute- dissection, trauma
Chronic- dilatation (Marfan’s, HTN)
Aortitis (syphilis, ankylosing spondylitis, vasculitis)

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12
Q

Eponymous signs of aortic regurgitation:

A

Quincke’s sign: capillary pulsations
De Musset’s sign: head nodding with each heartbeat
Corrigan’s sign: carotid pulsation
Duroziez’s sign: compress femoral artery 2cm proximal to stethoscope = systolic murmur
Traube’s sign: ‘pistol shot’ sound over femoral arteries

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13
Q

Difference between Austin Flint murmur and diastolic murmur of aortic regurgitation?

A

Early descending diastolic murmur = AR murmur

Mid diastolic crescendo murmur = Austin Flint (heard in severe AR)

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14
Q

Causes of aortic regurgitation:

Tension, been Conned, too much Rheum In it

A

Hypertension

Connective tissue: Marfans, Ehlers Danlos, osteogenesis imperfecta
Congenital: bicuspid valve

Rheum: seronegative arthritidies (ank spond, Reiter’s, psoriatic), rheumatoid arthritis, Takayasu’s

Infective: syphilis, rheumatic fever (strep pyogenes sequelae)

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15
Q

How is aortic regurgitation managed medically and definitively?

A

ACEi or ARBs to reduce afterload (systemic HTN)
Regular echo check ups- enlarging heart, LVEF, degree of AR

Surgery:
In chronic cases, replace the valve when:
Dyspnoeic + NYHA >2
Or ECG T wave inversion + EF <50% + pulse pressure >100mmHg

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16
Q

Commonest cause of mitral stenosis:

A

Rheumatic fever (commonest)

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17
Q

How small does the area of the mitral orifice have to be before a patient becomes symptomatic in mitral stenosis?

A

<2cm squared

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18
Q

If you hear a pansystolic murmur heard loudest at the apex, what investigations might you want?

A

ECG: AF + P mitrale (due to an enlarged heart)
CXR: pulmonary oedema, enlarged heart chambers (splaying of carina)
Echocardiogram + Doppler

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19
Q

What criteria is used to diagnose rheumatic fever?

A

Duckett Jones diagnostic criteria (Recent strep infection and 2M or 1M + 2m):

M:
Chorea, erythema marginatum, SC nodules, polyarthritis, carditis

m:
Pyrexia, arthralgia, PMH rheumatic fever,
Raised ESR, raised WCC, prolonged PR interval on ECG

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20
Q

If you wanted to prove a recent Group A beta haemolytic strep infection to diagnose rheumatic fever, what tests could you do?

A

Positive throat culture (normally -ve)
Rapid streptococcal antigen test +ve
Elevated streptococcal antibody titre (ASO or DNAse B titre)
Recent scarlet fever

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21
Q

Management of rheumatic fever:

A

Penicillin V

High dose aspirin- carditis/arthritis

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22
Q

A lateral thoracotomy scar may indicate which cardiac interventional procedure has occurred?

A

Mitral valvotomy- for mitral regurgitation

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23
Q

Why might a patient with mitral stenosis get a hoarse voice or dysphagia?

A

Enlarged LA atrium compressing the recurrent laryngeal nerve or the oesophagus

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24
Q

Causes of mitral regurgitation according to the valve leaflets, valve annulus (fibrous ring containing valves) + cordae pupillae

A

Valve leaflets:
Acute- endocarditis
Chronic- connective tissue disease (Marfan’s, Ehlers Danlos), myxomatous valves (stretchy valves), rheumatic fever

Valve annulus:
Chronic: calcification or LV dilatation stretching it, congenital ASD

Chordal papillae:
Acute- rupture ie MI
Chronic- fibrosis, amyloid

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25
Tricuspid regurgitation causes:
Commonest- LVF + pulmonary hypertension (functional) Endocarditis, rheumatic fever, carcinoid syndrome, congenital (ASD, Ebstein's, downward displacement of tricuspid valve)
26
What could a midline sternotomy scar indicate?
CABG- check radial artery + calves for saphenous vein harvesting Aortic valve replacement- opening click in systole, ejection systolic murmur Mitral valve replacement- closing click over S1, opening click in diastole
27
Potential interventions which would result in a lateral thoracotomy scar?
Mitral valve replacement Mitral valve valvotomy Coarctation repair/ BT shunt Lung pathology- pneumonectomy, lobectomy
28
Which valve problems can be treated with a valvuloplasty?
Mitral or pulmonary stenosis- where valves are pliable, non-calcified and non-regurgitant. Balloon catheter is inserted and inflated
29
Potential complications of valves:
Thrombosis (despite Warfarin) Bleeding (because of Warfarin) Haemolysis (RBCs against the valve) Infective endocarditis Early- S. epidermidis from skin. Late- S. viridians from blood Prosthetic dysfunction- LVF
30
Under what circumstances might an ICD be given prior to anyone having a cardiac arrest (primary prevention)
MI > 4 weeks ago + LVEF < 35% + Non-sustained VT + positive EP study Or + LVEF < 35% + broad QRS complexes OR Familial condition with risk of SCD (Brugada, HCM etc)
31
4 T's that cause constrictive pericardiris
``` Any cause of acute pericarditis TB: cervical lymphadenopathy Trauma: sternotomy scar Tumour, radioTherapy: thoracotomy scar connective Tissue disease: RA hands, SLE signs ``` Infection: viral (EBV, HIV, Coxsackie), bacterial, fungal
32
Dressler's syndrome?
Occurs 2-10 weeks after an MI, heart surgery or pacemaker insertion. Thought that myocardial injury stimulates formation of autoantibodies against heart muscle. PC: Recurrent fever + chest pain ± serositis (pleural/pericardial rub) Rx: NSAIDs, aspirin, steroids
33
Viruses that may cause acute pericarditis?
``` Coxsackie (can cause hand foot + mouth) Flu Ebstein Barr virus Mumps Varicella HIV ```
34
Which drugs may cause acute pericarditis?
Antiarrhythmic (procainamide) BP (hydralazine) Cromolyn sodium (anti-asthma) Isoniazid
35
In a patient with suspected constrictive pericarditis what signs might CXR uncover?
Calcified pericardium | Small heart
36
Difference between STEMI and NSTEMI in pathophysiology?
STEMI- clot of artery at site of a ruptured plaque | NSTEMI- clot of a ruptured plaque embolizes downstream to block a small artery
37
Following suspected ACS, how is GRACE score cut off used?
>3% mortality risk at 6 months = need intervention
38
What things cause a rise in troponin bar an MI?
PE, severe sepsis, heart failure, tachy/brady arrhythmias, extreme exertion, renal failure Gives a 5 x upper limit of normal
39
How does anticoagulation management differ according to acute or chronic AF?
CHADS2Vasc score is only used for chronic AF, if a patient has a score of 0 but wants to be DC-cardioverted then you should anticoagulate
40
How does Sotolol affect the ECG if given for AF?
Widens the QT interval, increasing risk of torsades de pointes
41
If someone has had AF for more than 48 hours and needs to be electively cardioverted, how long should you aim to anticoagulate for before doing so.
3 weeks
42
When is ivabradine used?
Patients with congestive heart failure who have tried beta blockers but can't slow heart rate down: Affects funny current in sinus node
43
Which patients get dysynchrony and how is it treated?
In patients with BBB, one ventricle contracts after the other due to slowed conduction leading to heart failure, so by pacing one ventricle early with a cardiac resynchronisation device.
44
What are the two ways ICD's can help abort dysrhythmias?
1. Shocking the heart | 2. Overpacing a tachycardia at 220bpm to make the heart depolarisation become refractory so it can take over pacing.
45
What are the 5 classes of anti-arrhythmic drugs?
``` 1- Na+ channel blockers (flecainide) 2- beta blockers 3- K+ channel blockers (amiodarone) 4- Ca++ channel blockers 5- Variable (digoxin) ```
46
What are the driving rules for angina and angioplasty?
Angina- no driving if Sx with rest or emotion | Angioplasty- stop driving for 1 week
47
What vision do patients require to allow for driving?
6/9 in the good eye | 6/12 in the bad eye
48
Signs of an atrial septal defect in adults aged 40-60?
As LV compliance reduces with age the L to R shunt is augmented. Pulmonary ejection systolic murmur Fixed S2 split Pulmonary hypertension (tricuspid regurgitation)
49
Causes of ventral septal defects?
Congenital or Post MI
50
Signs of VSD:
Pansystolic murmur, loudest at T area | Systolic thrill± parasternal heave
51
What is Eisenmenger's syndrome?
A L to R shunt reverses as pulmonary hypertension causes increased R-sided pressures. Results in cyanosis and heart failure
52
Where does coarctation of the aorta most commonly occur and what sign does this result in?
Distal to the L subclavian artery = radiofemoral delay Arteries leaving the aortic arch in order: Brachiocephalic A (splits into R subclavian and common carotid a) L common carotid L subclavian Alphabetical!
53
4 features of Tetralogy of Fallot:
Overriding aorta RVH Pulmonary stenosis VSD
54
Causes of acute pericarditis:
``` Vascular- MI Infection- viruses (coxsackie, flue, epstein barr, varicella), bacteria, fungi Trauma, surgery Autoimmune- Dressler's syndrome, RA, SLE, sarcoid Metabolic- hypothyroidism, uraemia Idiopathic Neoplasm- malignancy ```
55
Management of pericarditis:
1. Ibuprofen | 2. Colchicine (before steroids or immunosuppressants)
56
What are the complications of acute pericarditis:
Any cause of pericarditis may result in: Pericardial effusion Cardiac tamponade Chronic fibrosis + constrictive pericarditis (rigid pericardium)
57
ECG has low-voltage QRS complexes, they recently were admitted with viral pericarditis, what is the likely cause?
Pericardial effusion- attenuates electrical signals
58
Differences between constrictive pericarditis and cardiac tamponade:
Constrictive pericarditis- heart encased in rigid pericardium RHF, pericardial knock, prominant x descent on JVP CXR- small heart Cardiac tamponade- pericardial fluid raises chamber pressures Falling BP CXR- big globular heart Both have: Kussmaul's sign (JVP rising with inspiration) muffled heart sounds Pulsus paradoxus (BP drops by 10mmHg on inspiration, can't get enough blood to L side of heart when low lung pressure is compared to high chamber pressures)
59
How is acute myocarditis diagnosed?
Absence of MI, despite ECG changes and raised troponin I or T
60
Associations with dilated cardiomyopathy:
V: high BP I: viral M: Alcohol, haemochromatosis, thyrotoxicosis
61
Signs of HCM:
Jerky pulse Prominant a wave in JVP Systolic thrill at T area Ejection systolic murmur
62
How does empirical Rx for infective endocarditis differ if the valve is native of prosthetic?
Native: penicillin + vancomycin (inhibits peptidoglycan synthesis) Prosthetic: Vancomycin + gentamicin + rifampicin (Same if staph is cause)
63
Which bacteria make up the HACEK organisims accounting for 3% of endocarditis?
Gram -ve, treated with amoxicillin + gentamicin ``` Haemophilus Actinobaillus Cardiobacterium Eikenella Kingella ```
64
What are the signs of infective endocarditis and their pathological explanation:
``` Immune complex deposition: haematuria + glomerulonephritis Roth spots- fundi Splinter haemorrhages Osler's nodes (OWW! Painful pulps) ``` Embolic phenomena: Abscesses Janeway lesions (way!! High 5!! Painless palmar!!)
65
Tests for infective endocarditis:
``` FBC, CRP, ESR, U+E, Mg, LFT Urinanalysis (blood ++) CXR- cardiomegaly ECG- AV block (aortic root abscess) Echo- transthoracic if vegetations if >2mm, transoesophageal more sensitive for visualising mitral valve ```
66
Causes of tricuspid regurgitation:
T- tension in the pulmonary system > RV dilation R-rheumatic fever I- IE (IVDU) C- carcinoid syndrome + congenital
67
What is Ebstein's abnormality?
Downwards displacement of the tricuspid valve, small RV
68
Patient has a pansystolic murmur, loudest on inspiration, heard best at the L lower sternal border. Differential?
Tricuspid regurgitation Other signs: giant v waves in JVP, RV heave, pulsatile hepatomegaly, Pulmonary stenosis (should be louder higher up chest) or ASD- may get a split P2
69
Early diastolic murmur, loudest with inspiration, differential:
Tricuspid stenosis- opening snap | Pulmonary regurgitation- decrescendo
70
What is the Graham Steele murmur?
Decrescendo murmur in early diastole Pulmonary regurgitation Mitral stenosis Pulmonary hypertension
71
Heart defects associated with: Down's syndrome Turner's syndrome Marfan's syndrome
Downs- ASD, VSD, mitral regurgitation Turner's- Coarctation of aorta (webbed neck) Marfan's- mitral valve prolapse, AR, aortic dissection (midsystolic click)
72
Management of Aortic stenosis:
Symptomatic or Asymptomatic + peak gradient >50mmHg or valve area <1cm3 Open valve replacement Transcatheter AV implantation (TAVI) or valvuloplasty Valves: Metallic (anticoagulation needed, long lasting) Porcine valves (less durable) Cadaveric
73
What causes aortic sclerosis and how is it distinguished from aortic stenosis?
Age- related degeneration of the valve | No carotid radiation or pulse changes (character + volume), S2 normal
74
What is the Austin Flint murmur and what causes it?
Mid-diastolic low pitching murmur heard at the apex Sign of severe AR where backwards flow from aorta causes vibration against the mitral valve leaflet
75
Indications for aortic valve replacement in aortic regurgitation?
Increasing symptoms Enlarging heart- LVH T wave inversion in lateral leads
76
Causes of aortic regurgitation?
Ao- aortic dissection (acute) R- rheumatic fever, reiter's syndrome, rheumatoid arthritis T- Takayasu arteritis I- infective endocarditis C- connective tissue disorders (Marfan's, Ehler's Danlos)
77
Which valve abnormality causes a malar flush?
Mitral stenosis
78
What is a tapping apex beat associated with and why does it occur?
Mitral stenosis Left atrial hypertrophy pushes heart apex towards chest wall
79
An opening snap with S1 is assoicated with?
Mitral stenosis, as high volume of blood flowing through when it snaps shut
80
Indications for mitral valve balloon valvotomy
Symptomatic Or asymptomatic + Moderate to severe stenosis ( < 1cm^2/m2 body surface area) Pulmonary hypertension Not calcified pliable valves
81
Management of mitral stenosis:
Medical: AF common- rate control + anticoagulate Diuretics- reduce pulmonary venous congestion Surgical: Balloon valvotomy Open valve replacement (only if abnormal mitral valve shape or atrial thrombus likely to be dislodged)
82
Causes of mitral regurgitation?
``` Mitral valve prolapse Infective endocarditis Tendon rupture of tendinae chordinae (or papillary muscle) Rheumatic fever Annular calcification (elderly) LV dilatation (functional) ``` Connective tissue
83
What kind of imaging is needed for mitral regurgitation?
Trans-oesophageal echo + Doppler - TTE doesn't visualise the mitral valve well - can assess severity and suitability for repair (over replacement) - doppler assess size of regurgitant jet
84
Associations of mitral valve prolapse:
Mid-systolic click ± late systolic murmur Marfan's, osteogenesis imperfecta (blue sclera) Turner's syndrome, cardiomyopathy
85
What is rheumatic fever:
In 2% of the population, pharyngeal infection with b-haemolytic streptococci triggers rheumatic fever 2-4 weeks later when am antibody to the carbohydrate bacterial wall cross causes antigen mimicry with valve tissue
86
In rheumatic fever what provides evidence of Group B a haemolytic strep infection?
Throat culture (usually -ve 2-4 weeks post sore throat) Rapid strep antigen test +ve Rising strep antibody titre (ASO or DNAse B titre) Recent scarlet fever (strawberry tongue, macular truncal rash)
87
Major + minor criteria of rheumatic fever: | Jones criteria requires evidence of strep infection (antigen, ASO titre, scarlet fever, throat culture) +2M or 1M + 2m
M: CASES Carditis- CCF, cardiomegaly, murmurs, Arthritis- flitting polyarthritis of big joints Subcutaneous nodules Erythema marginatum- geographical raised red edges Syndenham's chorea- semi purposeful movements, unusual behaviour m: Fever, high ESR/CRP, PMH rheumatic fever Arthralgia or long PR interval (as long as these two aren't the major criterion)
88
Management:
Conservative: bed rest until CRP normal ``` Medical: Aspirin- carditis ± steroids Benzylpenicillin Constrict joint movement- severe arthritis Diazepam- chorea ```
89
Which valve is most damaged by rheumatic fever on average?
Mitral valves
90
What prophylaxis is given for rheumatic fever?
Penicillin V Given if carditis + persistent valve disease is present until age of 40 If no carditis- 10 years worth If no carditis or valve problems- 5 years until age 21 years
91
What are the cut offs for determining BP treatment?
Clinic reading is high = then ambulatory BP monitoring >135/85 mmHg + under 80 + comorbidity or risk Comorbidity:organ damage, CVS disease, renal disease, diabetes QRISK >20% >150/95: All patients
92
Lifestyle advice for hypertensive patients:
Diet: under 6g/day- ideally 3g/day Balanced diet, rich in fruit and veg Drink: less caffeine, less alcohol Quit smoking, exercise more
93
Drug management of hypertension:
ACEi or calcium channel blocker A+C A+C+D (indapamide not bendrofluthiazide) + aldosterone antagonist, alpha blocker, more thiazide (if K+ high)
94
SEs of dihydropyridine calcium channel blockers:
Nifedipine- ankle oedema, gum hyperplasia, flushes | Amlodipine- ankle oedema, tiredness, nausea
95
When is oral therapy recommended vs IV therapy for malignant hypertension?
Oral therapy normally unless CCF or encephalopathy Avoid sudden drops in BP (cerebral hypoperfusion, autoregulation is poor)
96
Patient has headache + seizures, BP is 210/120. | Aim of management?
Malignant hypertension encephalopathy Intra-arterial line for monitoring Get BP down to 110mmHg diastolic Furosemide IV Labetalol IV
97
``` BP targets for: A. Over 80s B. Under 80s C. Diabetic patients D. Proteinuric patients >1g/day ```
``` Clinic BP targets: A. 150/90 B. 140/80 C. 130/80 D. 125/75 ```
98
What is the pathological hallomark of malignant hypertension?
Vascular damage characterised as fibrinoid necrosis- fibrin like tissue in matrix
99
Signs ot look for in malignant hypertension?
Systolic BP >200 Diastolic BP >110 Fundi: papilloedema, bilateral retinal (flame) haemorrhages, exudates
100
Secondary causes of hypertension:
Renal: V Renal artery stenosis- atherosclerosis, fibromuscular dysplasia I- chronic pyelonephritis T- polycystic kidneys A- glomerulonephritidies, systemic sclerosis, PAN Endocrine: More salt + water retention- hyperaldoesteronism (Conn's) Very high cortisol mimics mineralocorticoid (Cushing's) Phaeochromocytoma, acromegaly, hyperparathyroidism Coarctation of aorta Drugs: steroids, the pill, MAOi
101
How can secondary causes of hypertension be examined for?
Cushingoid appearance- Cushing's Signs of renal disease- AV fistula, RRT (glomerulonephritis) Radiofemoral delay or weak pulses (coarctation) Renal bruit- stenosis Palpable kidneys- polycystic kidney
102
Tests for hypertension:
U+Es (cushing's, conn's), Ca++ (hyperparathyroidism) Glucose + cholesterol (risk stratify) ECG- LVH, past MI Urinanalysis- glomerulonephritidies ``` Special tests: urinary metanephrines (phaeo) 24 hours cortisol (Cushing's) Renal USS/ arteriography (RA stenosis) Renin aldosterone levels (hyperaldosteronism) ```
103
4 commonest causes of CKD:
1. Diabetes 2. Glomerulonephritidies (IgA commonest) 3. Unknown 4. Hypertension or renovascular disease 5. Pyelonephritis
104
4 stages of hypertensive retinopathy:
1. Silver wiring 2. AV nipping 3. Flame haemorrhages + cotton wool spots 4. Papilloedema
105
Management of chronic heart failure?
Conservative: stop smoking, reduce salt intake, optimise weight + nutrition, flu vaccine yearly, pneumococcal vaccine Medical: Treat cause (arrhythmia, valve issues) Treat exacerbating factors (anaemia, thyroid disease) Avoid exacerbating factors (NSAIDs- fluid retention, verapamil- negative inotropic effect) 1. ACEi AND B blocker (carvedilol, bisoprolol, nibivolol) 2. Spironolactone or hydralazine + nitrate or ARB (SHARDI) 3. Cardiac resynchronisation, digoxin, ivabradine (needs HR >75 and LVEF >35%) ± Furosemide for fluid overload
106
Rx for chronic intractable heart failure: Eg unresponsive oedema
1. Symptoms: Switch furosemide to bumetanide + Metolazone thiazide (SE: profound drop in K+) Opiates or IV nitrates 2. Bed rest, fluid + Na restrict Daily weights 3. TED stockings + DVT prophylaxis
107
What is the New York Heart Classification categories:
1. Heart disease present, no undue dyspnoea ordinarily 2. Comfortable at rest, dyspnoea on ordinary activities 3. Less than ordinary activities causes dyspnoea, which is limiting 4. Dyspnoea present at rest, all activity causes discomfort
108
What is the difference between ANP and BNP?
ANP is secreted from the atria BNP is secreted from the ventricle- related to the pressure in LV Used to discriminate between causes of SOB >100 is heart failure Higher the BNP = the higher the mortality risk
109
What causes systolic vs diastolic heart failure?
Systolic: LVEF < 50% MI, IHD, cardiomyopathy Diastolic: LVEF >50%, inability to relax Restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis, hypertension
110
Which symptoms occur in R-sided HF that do not occur in L-sided heart failure?
Peripheral oedema, ascites, facial engorgement Pulsation in neck + face (tricuspid regurgitation) Nausea + anorexia Epistaxis
111
Which symptoms occur in L sided heart failure, than may not occur in R sided HF (unless both sides involved)?
Dyspnoea, paroxysmal nocturnal dyspnoea, orthopnoea Wheeze, nocturnal cough ± pink frothy sputum Cold peripheries, weight loss, muscle wasting
112
Drugs which improve mortality in heart failure:
ACEi B-blockers Spironolactone Hydralazine* + nitrate *causes drug induced lupus- antihistone Abs
113
3 categories of low output heart failure:
Pump failure- systolic or diastolic (IHD, MI, cardiomyopathy etc) Excessive preload- mitral regurgitation, fluid overload (NSAIDs) Excessive afterload- aortic stenosis, hypertension
114
Causes of high output heart failure:
Output is unable to meet metabolic demands ``` Anaemia Pregnancy Wet beriberi (thiamine deficiency) Hyperthyroidism Paget's AV malformation ```
115
Tests for suspected heart failure?
FBC, U+Es, BNP CXR: alveolar oedema, B lines, cardiomegaly, dilated upper lobe vessels, pleural effusion ECG- ?cause Echocardiogram In essence if BNP + ECG abnormal > echo is warranted
116
What findings occur on a CXR in L-sided heart failure?
Alveolar shadowing- diffuse interstitial or alveolar bat wing shadowing Kerley B lines- interlobular septal oedema Cardiomegaly- cardiothoracic ratio >0.5 Diverted upper lobe vessels Pleural effusions
117
Framingham criteria of heart failure: 2M or 1M + 2m:
M: Paroxysmal nocturnal dyspnoea Neck vein distension Crepitations S3 gallop Hepatojugular reflux (rise in JVP 3-4cm = RVF) Acute pulmonary oedema Cardiomegaly Increased central venous pressure Weight loss of 4.5kg in 5 days of treatment m: Bilateral ankle oedema, nocturnal cough, dyspnoea on ordinary exertion Hepatomegaly, pleural effusion, tachycardia, 1/3rd decrease in vital capacity from max recorded
118
Indications for permanent pacemaker
Mobitz type II AV block (random dropped beats- higher risk) Complete AV block Symptomatic bradycardia Heart failure (3rd line, cardiac resynchronisation) Drug resistant tachyarrhythmias (SVT, VT)
119
Common triggers of AF:
``` HF, IHD, post MI (22%) PE, pneumonia, low K+ or Mg+ Mitral valve disease Hyperthyroidism, caffeine, alcohol 'Lone' = no cause identified ```
120
Tests for if a patient is found to have an irregularly irregular pulse:
U+Es (low K+ or Mg+), TFTs, cardiac enzymes ECG: no P waves, irregular QRS Echo: L atrial enlargement, mitral valve disease etc
121
How do you decide whether to cardiovert an unstable patient with AF if they have not been anti-coagulated?
If onset in < 48 hours: U+Es and cardiovert If onset in > 48 hours: 1. rate control with verapamil or b-blockers 2. transoesophageal echo to check thrombus free 3. give LMWH and then can cardiovert
122
Patient has has palpitations for the last 12 hours, they have chest pain and BP is 90mmHg. ECG shows fast AF. Four steps of management?
1. As under 48 hours, cardiovert: GA or IV sedation then 200J, 360J, 360J IV amiodarone as an alternative 2. Treat associated causes- MI or pneumonia 3. Rate control- Verapamil or bisoprolol 4. LMWH and calculate CHADsVasc score
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Chronic AF management:
Anticoagulate according to CHADsVas score ``` Rhythm control: elective cardioversion (anticoagulate for 3 weeks) or flecainide for normal heart, amiodarone if structural disease ``` Rate control: 1. B blocker or Ca+ channel blocker 2. + Digoxin or amiodarone
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Which factors favour rhythm control over rate control:
Symptoms or CCF Younger <65 years First presentation of lone AF or secondary to a precipitant (U+Es)
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Summarise the management strategies of new onset AF depending on stability of the patient:
<48 hours + unstable: DC cardiovert <48 hours + stable: rate control, anticoagulate*, TOE> cardiovert >48 hours + unstable: rate control, TOE, establish anticoagulation > cardiovert >48 hours + stable: as above, but wait 3 weeks for anticoagulation
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What is the pill in the pocket strategy for paroxysmal AF?
Can take sotolol or flecainide when AF comes on Only suitable if no LV dysfunction or IHD or valve disease Have systolic BP >100mmHg, HR >70 Ensure anticoagulation
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CHADsVasc score?
``` CCF Hypertension >140/80 Age- 65 (1), 75 (2) Diabetes Sex- female (1) Vasc- Stroke, TIA, VTE (2) ``` Score above 1 if male, or 2 if female warrants anticoagulation
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HASBLED score:
``` Hypertension >160mmHg Abnormal renal (1) or liver function (1) Stroke Bleeding propensity Labile INR Elderly >65 Drugs (NSAIDs, antiplatelets) + alcohol ```
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What causes a broad complex tachycardia:
1. Arrhythmia originating outside the normal conduction system 2. Abnormalities in the His-Purkinje system (BBB + SVT) 3. SVT conducted anterograde over a accessory pathway
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When is synchronised and unsynchronised cardioversion warranted in broad complex tachycardias?
VF or pulseless VT: unsynchronised DC cardioversion (200J-360J if biphasic) Stable VT: IV amiodarone DC cardioversion as 2nd line or if deterioration
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DRABC Rx for a stable broad complex tachycardia
``` A- oxygen B- ABG (if evidence of pulmonary oedema, sepsis, low GCS) C- U+Es, cardiac enzymes, Ca+, Mg+ Amiodarone IV MgSO4 if torsade de pointes ```
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What is Brugada syndrome?
An autosomal dominant condition which predisposes patients to sudden cardiac death from ventricular arrythmias due to sodium channellopathies. It is diagnosed by characteristic ECG changes
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In broad complex tachycardias, how are SVT + BBB differentiated from VT?
VT is more associated with: PMH of IHD Lack of response to adenosine ECG changes- positive QRS concordance in chest leads, left axis deviation, complete AV block
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Differential diagnosis of narrow complex tachycardia:
Sinus tachycardia Supraventricular tachycardia- AVRT or AVNRT Atrial tachycardia Atrial flutter Atrial fibrillation Multifocal atrial tachycardia- abnormal P waves Junctional tachycardia- may not see P waves
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CI to adenosine (used in stable narrow complex tachycardia):
Asthma 2nd/3rd degree heart block Smaller doses in transplanted hearts Antagonised by theophylline, potentiated by dipyridamole
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How does treatment of narrow complex tachycardia differ once type is identified:
Stable > vagal manoeuvres > adenosine 6g, 12g, 12g SVT: 2nd verapamil IV or b blocker IV Atrial flutter: treat as AF Multifocal atrial tachycardia: COPD associated, Rx hypoxia, verapamil Junctional tachycardia: b blocker or amiodarone or radiofrequency ablation
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ECG changes of wolff parkinson white syndrome?
Delta upstroke Short PR Wide QRS ST- T wave changes
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What are U waves associated with:
Hypokalaemia
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Things to look for in a patient with bradycardia:
Drug chart (b blocker, digoxin) Sick sinus syndrome- need to look for tachybrady syndrome Hypothyroidism Rx: if under 40bpm is atropine IV
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Difference between atropine and adenosine?
Adenosine- s for stop SVTs Slows conductance in AV node, adenosine R inhibits adenylyl cyclase, reducing cAMP, increasing K+ influx via rectifier K+ channels and hyperpolarising the cell Atropine- p for picks up the HR Competitive mACh R antagonist, inhibiting parasympathetic input
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A patient has an MI and develops 2nd degree heart block, what changes need to be made to their drug chart?
Increase rate of AV block: B blockers Calcium channel blockers
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In ectopic ventricular beats (pre-mature ventricular contractios) after an MI when would you investigate or treat further?
An isolated ectopic is fine. Non-Sustained Ventricular Tachycardia: at least 3 in a row with HR >100bpm NSVT within 48 hours of MI = no problem NSVT after 48 hours of MI = needs further investigation
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Who warrants an implantable cardiac defibrillator post MI?
VT + EF <35%
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What is Dressler's syndrome?
Autoimmune reaction to myocardial infarction PC: pericarditis, pleural effusions, fever, anaemia, high ESR 1-3 weeks post MI Rx: NSAIDs + steroids if severe
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Indications for a CABG:
For survival improvement: Left main stem disease Triple vessel disease (involving some of LAD) For symptom improvement: Refractory angina Unstable angina Unsuccessful angioplasty attempt
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CABG vs percutaneous coronary intervention
CABG- better resolution of angina, increased risk of stroke | PCI- reduced morbidity of operation + recovery time
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Which veins may be used for coronary artery bypass grafts?
Long saphenous vein | Internal mammary vein (look under pec margin)
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Post CABG management:
``` Conservative: Exercise- walk, cycle, swim, jog Drive at 1 month Reduce smoking + lipid intake Return to work at 3 months ``` Medical: Aspirin 75mg Anti-anginal drugs if angina Interventional: Angioplasty if angina reoccurrence is possible
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What ECG changes may constitute a STEMI?
ST elevation >2mm in chest leads or 1mm in limb leads New onset LBBB Posterior MI: horizontal ST depression + upright T waves in V1-3
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Medications to start post STEMI once PCI has been given?
ACEi within 24 hours b blocker Clopidogrel 300mg then 75mg Warfarin if large MI + risk of mural thrombus Aspirin 75mg Statin
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Immediate Treatment of NSTEMI:
Anticoagulation: Fondaparinux if no PCI in next 24 hours, otherwise LMWH High risk* GRACE score: Antiplatelet GPIIb/IIIa antagonist Tirofiban if PCI in next 96hr Clopidogrel after Low risk: Clopidogrel if risk >1.5%/year *high risk if persistent chest pain, ST depression, troponin up, diabetes aka NSTEMI
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Difference between NSTEMI and unstable angina?
+ Troponin also typically ST changes with unstable angina tend to be transient, whereas change with NSTEMI are more persistent
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A troponin level needs to be taken how many hours after an MI to exclude STEMI or NSTEMI?
6 hours, if normal and ECG normal at this point, very unlikely to be an MI
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In a patient presenting with angina, what rare causes may be considered as a differential?
Tachyarrhythmias, HCM, aortic stenosis Arteritis Anaemia
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Any differences in management of angina compared to post MI medical management?
No clopidogrel in angina 1. Add nitrates- GTN spray (SE: headaches, hypotension) 2. K+ channel activator (nicorandil) 3. Ivabradine if can't take b-blocker or Ca channel blocker
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Patient gets cardiac chest pain at rest, no normal cardiac risk factors. What could be the cause + Rx?
Prinzmetal angina: coronary artery spasm ECG changes of ST elevation resolve with pain Rx: Ca channel blockers ± long acting nitrates Avoid aspirin + b blockers, may increase vasospasm
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How should those with stable chest pain be investigated?
Determine the likelihood of coronary artery disease, based on age, gender, risk factors and symptoms Sx- typical anginal pain: 1. Constricting chest pain 2. Onsets with exercise 3. Relieved by rest or GTN within ~5 minutes High risk: smoking diabetic with hyperlipidaemia IHx according to calculated risk: 10-29% CT coronary artery calcification score 30-60% Functional: Myocardial perfusion scan Stress echo MR perfusion with contrast 60-90% Angiography >90%. Treat as coronary heart disease
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What alterations to U+Es do thiazides cause?
Low K+ and low Mg+ HIGH Ca+ (t-HIGH-azides) High urate- erk GOUT
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How do nitrates and hydralazine act differently?
Nitrates (and a-blockers) dilate veins and large arteries = lower preload Hydralazine dilates the resistance vessels, aka arterioles = lowers afterload + systemic BP
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At least how many hours post dose should you check Digoxin levels?
6 hours
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What does Digoxin toxicity cause?
Confusion Nausea + anorexia Yellow vision Any arrhythmia
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How do statins work?
Statins inhibit the enzyme HMG-CoA reductase to prevent cholesterol recycling, more has to be made de novo, reducing levels as LDL receptor expression by the liver increases. Most effective at night when cholesterol metabolism happens most.
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SEs of statins:
Muscle aches Abdo discomfort LFTs- only act if ALT 3x baseline Myositis, rarely rhabdomyolysis
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Cautions + CIs for ACE inhibitors:
PC: high K+, low Na+, hypotension, hypovolaemia PMH: pregnancy, LVOT, severe COPD/cor pulmonale Renal artery stenosis Less advisable where patients have CKD + may be at risk of AKI
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ACEi side effects:
Dry cough Low BP- best to take at night first time Taste disturbance Renal impairment Check U+Es before and after starting.
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Describe coronary angiography:
Insert a small tube from a vein or radial/femoral artery to access the heart. Measure pressures, look at cardiac anatomy, biopsies, put valve in. Before: NBM for 6hrs before, blood tests ``` Risks: Bleeding Reaction to contrast Angina + arrhythmias Infection ``` Alternative: CT angiography can rule out CAD well
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What is exercise testing for cardiac ischaemia:
ECG + BP monitoring whilst on a treadmill with increasing difficulty, look for ST changes (down sloping ST depression) Used to confirm suspected diagnosis of IHD or assessment of exercise-induced arrhythmias CI: severe aortic stenosis, uncontrolled HTN/ HF/ arrhythmia, acute myocarditis or pericarditis, acute aortic dissection/ PE Hard to interpret: musculoskeletal exercise limitations, pacemaker patients, LBBB or AV block already ``` Stop the test if: chest pain, dyspnoea, cyanosis, pallor Feeling faint or exhausted ST elevation in leads Arrhythmia Development of AV block or LBBB 90% max heart rate achieved ```
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Where do you place chest leads in ECG:
V1-2: 4th intercostal space, sternal edges V4: 5th intercostal space, mix clavicular V3: between them V5: same horizontal plane of V4 but anterior axillary V6: same plane but mid axillary Ride (RA) your (LA) green (LL) bike (RL)
169
How is an incomplete bundle block different from a complete block on ECG?
Incomplete = less than 0.12secs
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What causes RBBB on ECGs?
Normal variant PE Cor pulmonale
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What causes LBBB on ECGs?
IHD Hypertension Cardiomyopathy Idiopathic fibrosis
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How does LVH look on ECG compared to RVH?
LVH: (S in V1) + (R in V6) > 35mm Or (R in V6) > 25mm
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Which leads show ST elevation with the different types of MI and which arteries are affected?
II, III, aVF = inferior (R coronary) V1-4 = anteroseptal (left anterior descending) V4-6, aVL = anterolateral (LAD ± circumflex) Tall R, ST depression in V1-2 = posterior (circumflex)
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What kind of ECG rhythm has regular normal QRS complexes, but no P wave?
Nodal rhythms (AVN rather than sinus node)
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How does the deflection in Leads I, II and III demonstrate axis deviation and what degrees are associated with each?
L axis- leaving: I up, II down, III down (-30 to -90) However if I is up, III down and II isoelectric (0- -30) = physiological R axis- reaching: I down, II up, III up (90- 180) Extreme axis- v odd: I down, II down, III down (-90 - 180)
176
What features can be discerned on an ECG from the shape or absence of P waves?
Absent: AF, AV nodal rhythm, sinoatrial block Mitrale (bifid): delayed conduction- LA hypertrophy Pulmonale: peaked P waves- RA hypertrophy (can occur in low K+) >2.5mm, seen in leads II, III, aVF NB these P wave changes may only be visible in a couple of leads
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Normal range for PR interval:
0.12-0.2s (3-5 squares) Short- accessory pathway Long- AV block
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What features make up a normal Q wave?
< 2 squares deep < 1 square wide Seen in V5-6, aVL (as heart normally depolarises left to right) If Q waves not meeting these criteria, may occur within a few hours of MI
179
Which drugs cause prolongation of the QT interval?
``` STOP hEARt Sotolol Tricyclics Over the counter antihistamines Phenothiazines (typicals) ``` ``` (Hypo K+, Ca+, Mg+) Erythromycin Amiodarone (Romano-Ward Temp low) ```
180
How is corrected QT interval calculated?
QTc= QT/ square root (RR) Corrected for RR
181
What are Romano Ward and Jervell + Lange Nielsen syndrome associated with and how do they differ?
Both due to K+ channelopathy Long QT syndrome, increasing risk of VT, VF, torsades Romano-Ward autosomal D JLN- autosomal R, get congenital sensorineural hearing loss also
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What is the J wave on an ECG and what is it associated with?
Hypothermia, subarachnoid haemorrhage + hypercalcaemia Positive deflection at end of QRS (QRS-ST junction)
183
In a patient with LBBB, how does the axis deviation indicate whether it is the anterior or posterior fascicle that is blocked?
L anterior hemiblock= left axis deviation L posterior hemiblock = right axis devation Anterior fascicle conducts to the upper anterior regions, whereas the posterior fascicle conducts inferior + posterior With the fascicle blocked, the eventual depolarisation of these areas happens later and requires a large wave of depolarisation, hence as the L anterior gets depolarised late = left axis deviation As the bottom of the heart gets depolarised late = right axis deviation
184
Aside from polycystic kidney disease what are the other risk factors for a Berry aneurysm?
Ehlers- Danlos Marfan's Neurofibromatosis Smoking Hypertension
185
Name some non-genetic causes of dilated hypertrophic cardiomyopathy:
HAMS: Haemochromotosis Alcohol Sarcoid (Duchenne + muscular dystrophy)