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Y3 Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

How should arrhythmias be investigated?

A
  • bloods: (TFTs, U&Es, glucose, FBC)
  • baseline ECG without symptoms
  • Echo (not diagnostic)
  • 24 hr ECG
  • implantable loop recorders
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2
Q

When do you worry about ectopic beats on a 24hr ecg?

A

when they occur >20% of the time, it may lead to heart failure

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3
Q

Describe how regular narrow complex (SVT) regular tacharrhythmias are treated if the pt is haemodynamicaly stable? (4 steps)

A

1st: Valsalver maneouvre
2nd: carotid sinus massage
3rd: adenosine 6mg IV then 12mg x2
4th: IV verapamil or betablockers(last resort// in asthma)
5th: electrocardioversion (do this 1st if haemodynamically unstable)

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4
Q

How should narrow complex irregular tachycardias be treated initially?
(if haemodynamically unstable// adverse signs, if new onset within 48hrs, if been present for >48hrs and if infrequent episodes)

A

Treat as AF- by far most likely diagnosis
Haemodynamically unstable/ adverse signs: synchronised DC
Acute presentation (within 48hrs): chemical rhythm control with amiodarone (if they have structural heart disease) or 300mg PO flecainide then DC and if urgent rate control needed use CSM, VSM, bisoprolol then verapamil
If old: anticoagulate and offer bisoprolol/ verapamil for rate control/ digoxin in HF. Then bring back in two weeks for cardioversion. Flecainide PRN can be used in infrequent symptomatic AF.

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5
Q

What are the criteria on the CHA2DS2 VASc score?

A 
Congestive heart failure/ LVSD
Hypertension 
Age >75 (scores 2)
Diabetes 
Stroke/ TIA/ VTE (scores 2)
Vascular disease 
Age 65-75
Sex -female
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6
Q

What are the adverse signs in tachy/brady which indicate you may need to use a defib

A

shock
MI/ chest pain/ ischaemia on ECG
Heart failure
Syncope
Synchronised DC shocks for tachy, transcutanous pacing for brady.
Electrical cardioversion before chemical (amiodarone) for tachy. Chemical (atropine) before electrical for brady.

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7
Q

Name 3 anticoagulants

A

warfarin, apixaban, dabigatran, rivaroxaban

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8
Q

What can be done in AF if anticoagulants are not tolerated or contraindicated?

A

left atrial appendage occlusion

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9
Q

Give 5 causes of AF

A
  • hypertension
  • valvular disease
  • heart failure
  • IHD
  • chest infection
  • PE
  • lung cancer
  • alcohol
  • hyperthyroid
  • electrolyte disturbance
  • infections
  • diabetes
  • age
Can also remember by mnemonic PIRATES: 
Pulmonary embolism.
Ischaemia.
Respiratory disease. - lung cancer, chest infection
Atrial enlargement or myxoma.
Thyroid disease. (Hyper)
Ethanol.
Sepsis/sleep apnoea.
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10
Q

How are unstable bradycardia treated?

A
  • 500micrograms atropine IV every 3-5 mins (upto 6 times)
  • If unsatisfactory response/ recurrance, use transcutanous pacing (may need anaesthetist to sedate) or transvenous pacing if cardiology available
  • is delay for this, use isopraline or adrenaline
  • find and treat cause (eg electrolyte disturbance)
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11
Q

How should pulseless VT and V fib be treated?

A

defibrillation

adrenaline 1mg every 3-5 mins and amiodarone 300mg after 3 shocks +/- lidocaine

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12
Q

How should

a) unstable
b) stable sustained VT with a pulse be treated?

A

unstable: sedate and do DC cardioversion x 3 then amiodarone 300mg over 20 mins whilst doing more DC shocks, check and correct electrolytes
stable: amiodarone, then flecainide then lidocaine then cardioverision or pacing

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13
Q

How can non sustained VT be treated?

A

beta blockers- may also need implantable defibrillator

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14
Q

What is torsades de pointes? (2) What are the ECG features?

A

Type of polymorphic ventricular tachycardia
Associated with long QT.

Features: changes in amplitude (twisting) of the QRS complexes around the isoelectric line.

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15
Q

How is torsade de pointes treated?

A

IV magnesium sulphate 2g given over 10 minutes
(initially and then can be repeated after 5-15 mins)

if unsuccessful then sedate for DC cardioversion
Look for cause of long QT (drugs, hypokalaemia, bradycardia, genetics)

Other anti-arrhythmics cant be used as they prolong QT

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16
Q

What investigations are needed for angina

A
  • ECG: pathological q waves, LBBB, ST segment changes, T flattening or inversion
  • Bloods: (FBC (anaemia), U&E (renal function), glucose and cholesterol (RFs), LFTs (statins), Troponin if ECG changes or unstable
  • Echo to asses function or if HCM or valve disease is suspected
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17
Q

How should stable angina be treated? (8)

A
  • all need referral to cardio via rapid access chest pain clinic
  • GTN spray for symptom relief
  • aspirin (75-300mg) or clopidogrel for anticoagulant taking into account bleeding risk
  • statins and other CVS risk reduction (HTN treatment, stop smoking etc)
  • BB or CCB first line antianginal, long actingin nitrates and ivrabradine can be used as additional or alternative to these. add a 3rd only when waiting for revascularization therapy
  • ACEi if CKD/HTN/T2DM/ heart failure/ previous MI
  • cardiac rehab (exercise)
  • coronary revascularisation if high risk or medical therapy fails on two anti anginal medications, consider CABG when ok on medical therapy but left main stem or proximal 3 vessel disease
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18
Q

How is an MI investigated?

A
  • ECG
  • Bloods: FBC, U&E, glucose, lipids, crp, troponin T and I and cardiac enzymes
  • CXR
  • pulse oxymetry
  • cardiac catheterisation and angiography
  • Echo
  • MI perfusion scan / CTCA
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19
Q

How should a STEMI be treated?( short term- inc drug doses)

A
  • Aspirin (300mg) and ticagrelor (180mg) (or clopidogrel 300mg) PO
  • IV Morphine (5-10mg)
  • IV metaclopamide (anti emetic) 10mg
  • GTN sublingual or IV (50mg in 50 ml NS at 2-10ml/hr)
  • Oxygen if sats are low (<94%)
  • call cathlab for primary PCI or CABG if multi vessel disease, if no PCI available within 120 mins of presentation then FIBRINOLYSIS
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20
Q

What do you need to think about when assessing NSTEMI risk and need for angiography/ PCI? (6)

A

Calculate GRACE SCORE

  • rise in troponin
  • dynamic st or t wave changes
  • HR, BP and age
  • If arrested at any point
  • diabetes
  • CKD
  • LVF
  • recent PCI or prior CABG
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21
Q

What causes mitral regurg and mitral stenosis?

A

Regurg: MI, LV dilation, calcification, CT disorders, rheumatic fever, endocarditis, cardiomyopathy
Stenosis: rheumatic fever (most common cause!) or congenital (rarer)

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22
Q

What causes aortic stenosis and regurg?

What is the most common cause of aortic stenosis in someone <60yrs?

A

Stenosis: calcification, sometimes rheumatic fever or congenital
Regurg: congenital, CT disorders, rheumatic fever, RA, SLE, hypertension

Most common cause of AS <60yrs = bicuspid arotic valve

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23
Q

Describe the clinical features of mitral regurg?

A

Dyspnoea, fatigue, palpitations, AF, systolic murmur (pan-systolic) best on expiration at apex with soft s1,

Displaced Apex Beat
Cardiomegaly
Acutely: presents with pulmonary oedema

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24
Q

Describe the clincial features of mitral stenosis?

A

pulmonary hypertension–> dyspnoea, haemoptysis, chronic bronchitis like picture, RA pressure increase can impinge recurrent laryngeal so hoarseness of voice, dysphagia. Fatigue, palpitations, chest pain, systemic emboli, rarely infective endocarditis. Malar flush on cheeks, AF, diastolic murmer best on exp with loud s1.

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25
Q

Describe the clinical features if Aortic stenosis

A

chest pain, exertional dyspnoea or syncope, heart failure, heaving, displaced apex, aortic thrill, ejection systolic murmer radiating to carotids.

slow rising pulse
haemolytic anaemia
loudest on expiration when sitting forwards

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26
Q

Describe the clinical features of aortic regurgitation.

A

exertional dyspnoea, PND, Orthopneoa, palpitations, angina, syncope, collapsing pulse, displaced apex, high pitched early diastolic murmer, quinckes sign, de musset’s sign

Quincke’s sign =nail bed pulsations
De Mussets = head bobbing

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27
Q

How are valvular diseases investigated?

A

Gold Standard = Transthoracic Echocardiography

ECG, FBC, CXR, cardiac catheterisation

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28
Q

how do you treat valvular diseases?

A

balloon valvuloplasty or open valvulotomy for stenosis or valve replacements for both

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29
Q

Describe the clinical features of left sided heart failure

A
  • Breathlessness (PND &orthopnoea v specific to it) +/- nocturnal cough and wheeze,
  • fatigue
  • pink throthy sputum
  • increased HR and RR
  • exertional dyspnoea
  • bibasal coarse crackles
  • murmers associated with cause
  • cardiomegaly

Can present acutely with acute onset breathlessness

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30
Q

What investigations are needed for heart failure?

A

ECG and BNP, if either abnormal do echo. If had MI before and NT-proBNP is really high - Refer for 2 week echo!

Bloods: FBC, U&E, LFT, glucose, fasting lipids, TFT, cardiac enzymes
CXR (cardiomegaly, alveolar shadowing, fluid in interlober space (kurley b lines), pleural effusions)
Urinalysis (? Nephrotic syndrome). Cardiac MRI (rarely), Ct angiography if CHD suspected as cause

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31
Q

Describe Class I to IV of the NYHA heart failure severity classification

A

Class1: no symptoms on ordinary physical activity
Class2: slight limitation of physical activity by symptoms (walking up stairs)
Class3: Less than ordinary activity leads to symptoms (walking on flat ground)
Class4: inability to carry out any activity without symptoms (changing clothes)

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32
Q

How can heart failure be managed pharmacologically?

A

Diuretics: furosemide 40mg to relieve symptoms, add thiazide if no improvement but monitor k+ (systolic and diastolic)
ACEi: in those with LV systolic dysfunction, ARB if get a cough
B Blockers: decreases mortality, ‘start low and go slow’ (systolic)
Consider starting antiplatelet and statin (will be indicated in many)
SECONDARY CAR MANAGEMENT:
Spironolactone: use in those still symptomatic despite optimal therapy and in those post MI with LVSD (systolic) - also has MAJOR prognostic benefits! :)
Digoxin: Use in those with LVSD who are still symptomatic despite optimal treatment
Vasodilators: hydralazine and isosorbide dinitrate should be used if intolerant to ARB or ACEi
Ivabradine used in NYHA class 2-4 with sinus rhythm >75bpm and conventional therapy not working/ tolerated and ejection fraction <35%
SGLT2 inhibitors: improves prognosis in LVSD

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33
Q

How is heart failure managed non pharmacologically?

A

Care Plan inc. info and support
Optimise risk factors - stop smoking and drinking
Treat cause
Flu vaccines should be given
Salt and fluid restriction (if needed)
Cardiac rehabilitation
LV assist devices can be used in end stage

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34
Q

When should urgent and 6 week referrals be used when heart failure is suspected?

A

Urgent referral if: previous MI, very high BNP, severe symptoms, pregnant
6 week referral: no Mi history but reasonably high BNP, ECG abnormal, ECG normal but strong suspicion of heart failure.

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35
Q

How is flash pulmonary oedema managed? (inc drug doses)

A
  • Furosemide 40-80 mg IV slowly to remove fluid
  • High flow O2 (if <94%)
  • Sit up
  • Morphine 5mg IV to help with feeling of breathlessness (CI in liver failure and COPD)
  • GTN spray 2 puffs for veno dilation (CI if BP is LOW - can cause hypotension
  • Do BNP, ECG, CXR, echo, troponin, U&E, daily weights, obs QDS
  • be aware of copd, asthma attack and pneumonia as differentials
  • If these fail, CPAP and IV nitrates
  • If BP drops <100mmHg treat as cardiogenic shock (inotropes)
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36
Q

Give 3 renal causes of secondary hypertension

A

glomerularnephritis, systemic sclerosis, pyelonephritis, APCKD, renovascular disease

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37
Q

Give 3 endocrine causes of secondary hypertension

A

cushings, conns, thyroid, phaeochromocytoma, acromegaly, hyperparathyroidism

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38
Q

Give 3 non endocrine or renal causes of secondary hypertension

A

pre eclampsia
coarcation of aorta
obstructive sleep apnoea
pharmacological (alcohol, cocaine, amphetamines, antidepressants, COCP, ciclosporin, EPO, steroids)

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39
Q

What are the risk factors for primary hypertension

A

High BMI, high salt diet, lack of activity, excess alcohol, stress, old age, FHx, ethnicity, gender (F>M)

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40
Q

How would unexplained hypertension be investigated? (10)

A
  • Ambulatory blood pressure monitoring
  • Urine dip for protein and blood (renal disease)
  • Serum creatinine, U&E, eGFR
  • Renal USS
  • 12 lead ECG
  • Echo
  • Fasting blood glucose and lipid profile
  • Urinary free cortisol/ dexamethasone surpression test
  • Renin/ aldosterone levels
  • Plasma calcium
  • MRI of renal arteries
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41
Q

How is emergency hypertension (>200mmHg systolic) managed?

A
  • IV nitroprusside or nicarpidine
  • phentolamine for phaeochromocytoma crisis
  • Find cause
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42
Q

What lifestyle advice can be given to reduce blood pressure

A

weight reduction, whole grain starchy foods, increase activity, low sat fat, fruit and veg, low caffine, low alcohol, stop smoking, low salt

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43
Q

When should drugs be used for treatment of hypertension

A
  • everyone in stage 2 (>160 clinic and >150 ABPM) and stage 1 (<140 clinic and <135 ABPM) if <80 yo, plus signs of end organ damage or DM or QRISK2 >20%.
  • Refer is step 4 (resistant HTN) not bringin it down to <140
44
Q

Describe secondary causes of hyperlipidaemia (5)

A
  • hypothyroid
  • liver disease
  • nephrotic syndrome
  • cushings
  • drugs (thazides, steroids, ciclosporin, beta blockers, COCP, antipsychotics)
45
Q

What criteria are used to diagnose someone with a familial hyperlipidaemia?

A 
Simon broom diagnostic criteria:
- TChol> 7.5 mmol/l
plus
- tendon xanthoma in pt or evidence of in a 1st or 2nd degree relative 
OR
- DNA evidence
46
Q

How is hyperlipidaemia investigated?

A
  • lipid profile (fasting test)
  • fasting blood glucose and hba1c
  • renal function
  • LFTs
  • TFTs
  • DNA test if familial mutation suspected
  • creatine kinase (baseline for statin therapy)
47
Q

What dose of atorvastatin is used for primary and second prevention?

A

primary: 20mg
secondary: 80mg

48
Q

What are the main side effects of statins?

A

Myalgia (no raised CK) and rhabdomyalysis (usually starts within 6 months, stop drug if muscle pain not tolerable or CK >10x the upper limit of normal) and hepatotoxicity (reversible, monitor LFTs)

49
Q

Give 4 alternatives to statins

A

ezetimibe (cholesterol lipase inhibitors) , fibrates (PPAR agonists) , nicotinic acids (inhibit lipoprotein synthesis), evolocumab (destroy LDL receptors)

50
Q

What can cause infective endocarditis? (5)

A
  • valve trauma (catheters, pacing wires)
  • dental procedures
  • valve replacement
  • valve pathology
  • thrombus formation
  • CKD
  • SLE
  • neoplasia
  • malnutrition
  • cuts
  • IV drug use (tricuspid)
  • nothing at all
51
Q

Which valves are most commonly affected by infective endocarditis?

A

Mitral> aortic > both mitral and aortic > tricuspid> pulmonary
tricuspid is most common in IVDU

52
Q

Which organisms most commonly cause infective endocarditis? (3)

A

staph a, strep viridans, enterococcus

53
Q

What are the major dukes criteria for diagnosing infective endocarditis? (2)

A

+ve blood culture (at least 2)

+ endocardial involvement (+ve echo, new regurg, abscess)

54
Q

What are the minor dukes criteria for diagnosing infective endocarditis? (5)

A
  • predisposing condition
  • fever
  • immunologic or vascular signs
  • one positive blood culture
  • positive echo not meeting major criteria
55
Q

What signs are associated with infective endocarditis?

A
  • roth spots on retina
  • splinter haemorrhages
  • janeway lesions (lesions on palms)
  • oslers notes (nodes on fingers)
56
Q

How is infective endocarditis treated?

A
  • IV abx (amoxicillin or gentamicin) start treating empirically while you wait for cultures to return
  • If prosthetic valve is cause, it will need replacing if abx dont work or they develop heart failure
  • gent + vanc + rifampicin if prosthetic valve
57
Q

How may hypertrophic obstructive cardiomyopathy (HOCM) present?

A
  • asymptomatic
  • palpitations
  • chest pain
  • syncope
  • breathlessness
  • tiredness
  • sudden cardiac death
58
Q

What ECG findings may be present in HOCM?

A

tall sharp q waves in anterior leads

59
Q

What is heard on auscultation of HOCM?

A

systolic creshendo- decreshendo murmer heard best on left sternal edge and when performing the valsalva manouver

60
Q

How is HOCM treated medically?

A

B Blockers, CCBs, anticoagulants and diuretics if in heart failure

61
Q

What surgical treatment is available for HOCM? (2)

A
  • implantable cardioverter defibrillators are used in high risk pts (age, thickness, fhx sudden cardiac death, syncope, VT)
  • septal alcohol ablation and surgical myectomy also available but carry risks such as BBB, arrhythmias, death
62
Q

What does QRISK2 take account for? (13)

A

age, gender, diabetes, familly history, blood pressure, postcode, BMI, cholesterol, ethnicity, rheumatoid, CKD, AF

63
Q

What dietary recommendations would you make to reduce someones cardiovascular risk?

A
  • total fat is <30% energy intake
  • saturated fats <7% of energy intake
  • wholegrain diet (brown bread rice etc) w/ starchy foods
  • reduce sugar intake
  • increase fruit veg, fish, nuts/ seeds/ legumes intake
64
Q

Other than dietary changes, give 6 recommendations you’d advise to reduce someones cardiovascular risk

A
  • get 150 mins moderate
    intensity aerobic or 75 mins vigorous exercise a week
  • get to health BMI by reducing calories
  • reduce alcohol intake to 2-3 units per day
  • stop smoking
  • statins
  • blood pressure control
65
Q

How do you report on an ECG in an osce?

A

PRAIRS
P: pt- check name, time and date of ECG
R: rate and rhythm
A: axis deviation
I: intervals: PR 3-5 small squares, QRS 2-3 small squares, QTc 400-450 ms, check the P, QRS and T waves morphology
R: R wave progression from V1-6
S: ST segment (T wave present? tall and tended? ST elevation or depression? T wave inversion?)

66
Q

Describe normal and right and left axis deviation?

A

Normal: I, II or AvF should be most +ve
Left axis: AvL is most positive
Right axis: III is most positive

67
Q

What could cause poor R wave progression?

A
  • prior anteriorseptal MI
  • LVH
  • RVH
  • dilated cardiomyopathy
  • incorrect lead placement
68
Q

Describe the appearance of left bundle branch block?

WILLIAM

A
  • wide QRS
  • wide negative in V1 sometimes with W shape
  • wide positive in V6 with M shape
  • Left axis deviation and poor R wave progression also associated
69
Q

Describe the appearance of right bundle branch block?

MARROW

A
  • wide QRS
  • M shape and wide QRS in V1
  • W shape and wide in V6
70
Q

Describe how you approach tachycardias?

A

1st: wide or narrow QRS?
2nd: Regular or irregular rhythm?
3rd: if narrow QRS-> P waves?
4th: if broad QRS-> delta waves? (indicate abnormal atrial- septal connection)

71
Q

What is the cause of a tachycardia with narrow complex QRS, regular rhythm but no P waves?

A

AV node reentry tachycardia or AV reentry tachycardia

also usually see inverted P in II, as atria depolarising from AV node not SAN

72
Q

What features do you look for when you suspect VT?

A 
Wide QRS
tachycardia
irregular or regular 
capture beats 
fusion beats 
Ventricular- Atrial dissociation
73
Q

Describe the method for assessing an ECG with bradycardia? (4)

A
  • Look at QRS width to asses where escape rhythm arises
  • Are there P waves? (is SAN or AVN causing contraction)
  • Is there a relationship between P and QRS
  • Any pacing spikes suggesting a pace maker
74
Q

What is bi and triphasicular block on an ECG?

A

Biphasicular block: RBBB + Left axis deviation

Triphasicular block: RBBB+ left axis + prolonged PR interval

75
Q

What would an ECG look like if the escape rhythm is arising from high in the bundle of his in 3rd degree heartblock?

A

Narrow but shallow QRS

No P- QRS association

76
Q

What should an ECG look like is the escape rhythm is arising from the right or left ventricle?

A

QRS is wide for both and negative if arising from right ventricle and positive if arising from left ventricle.
No P- QRS association

77
Q

What does an ECG look like if there is only one pacing lead?

A

Pacing spike before QRS, QRS is wide and negative as lead is placed in RV

78
Q

Describe how a STEMI ECG may change over time

A
  • ST elevation over mins- hrs
  • T wave inversion, Q wave development and ST elevation persisting over hrs to days
  • Q wave and T wave inversion can persist for a week as ST elevation goes down
  • Q wave can persist for months, T wave inversion reverses
79
Q

What leads would be affected by an inferior MI and which vessel is affected

A

II, III, AVF

RCA and/or LCx depending on which one is dominant in that area

80
Q

What leads are affected in a lateral MI and which vessel is affected?

A

I, aVL, V5-6

Left circumflex or diagonal of LAD

81
Q

What leads are affected in a anterior MI and which vessel is affected?

A

V1-4

left anterior descending

82
Q

What reciprocal changes are seen on ECG of anterior MI

A

ST depression in II, III and aVF

83
Q

Where is the occlusion of V3-6, II, III and AvF are affected by ST elevation?

A

Left main stem (takes out circumflex and LAD)

84
Q

ST elevation is often seen normally in LBBB, what criteria are used to determine if it is truly an MI?

A

sgarbossa criteria

85
Q

How do posterior STEMIs present?

A

ST depression in V1-6–> may need todo a V7-9 to see ST elevation

86
Q

Describe the types of heart block

A 
1st- prolonged PR
2nd: 
mobitz1/ wenkebach: increasing PR interval with each beat until a QRS is dropped (regularly irregular)
Mobitz2: random non conduction of a  QRS
3rd: complete dissociation
87
Q

how is 1st degree heartblock managed?

A

Its usually benign. Check meds for cause: CCB, betablockers, cholinergics.
if slow can give atropine

88
Q

How is 2nd degree heartblock managed?

A

Mobitz1: usually benign

Mobitz 2: needs implantable pacemaker insertion, usually temporary wire first, then permanent one fitted later

89
Q

How is 3rd degree heartblock managed?

A
  • if very slow can give atropine

- also needs transvenous temporary pacing followed by permenant pacemaker insertion

90
Q

What causes LBBB?

A

Usually systemic things causing LVH eg high blood pressure, aeortic stenosis. Can also get primary conduction problems

91
Q

What causes RBBB?

A

Things causing right ventricle strain, eg PE, corpulmonale, MI, pulmonary hypertension

92
Q

What causes long QT?

A

HYPOs: hypokalaemia/ calcaemia/ magnesia
idiopathic
drugs: amiodarone, erythromycin
LVH, MI, heart failure

93
Q

What causes short QT syndrome?

A

digitalis toxicity
hyperkalaemia/ magnesia/ calcaemia
idiopathic

94
Q

Give 4 complications of MI

A 
ALARMS
Aneurysm 
LV dysfunction 
arrhythmias
rupture 
Mitral regurg
septal defect 
ALSO: tamponade, death, embolism, Dresslers syndrome,
95
Q

What may cause heart block?

A
  • CCBs
  • amiodarone
  • sick sinus syndome
  • inferior MI
  • myocarditis
  • digoxin
  • B blockers
96
Q

What is sick sinus syndrome? What is the management?

A

SAN fibrosis in elderly, leads to a range of arrhythmias inc AF, tachy- brady, sinus pauses. most of which need permanent pacemakers

97
Q

How should AF be investigated?

A
  • Echo- may find cause eg mitral valve disease, LA enlargement etc and for assessment of LV function
  • U&E
  • TFTs
  • ECG
98
Q

Describe the clinical features of right sided heart failure

A
  • peripheral odema and associated weight gain
  • ascites
  • increased JVP
  • anoerxia and GI complaints
  • most have PND, orthopnoea, dyspnoea etc as most right sided heart failure is caused by left sided heart failure
99
Q

What causes right sided heart failure?

A
  • most commonly its caused by left sided heart failure
  • some due to increase pulmonary pressure
  • this can be idiopathic or secondary to diseases like COPD (if this is cause of pulmonary HTN its called cor pulmonale)
  • some is due to valvular disease
100
Q

What causes left sided heart failure? (give 3 systolic and 3 diastolic)

A 
Systolic: 
- HTN
- Coronary artery disease (ACS)
- idiopathic dilated cardiomyopathy
- mitral or aortic regurg
Diastolic:
- HTN
- HOCM
- aortic stenosis
- tamponade
- obesity 
- ACS
101
Q

Describe the clinical features of pericarditis?

A
  • central chest pain worse on lying flat, relieved by sitting forward
  • percardial rub
  • fever
  • signs of tamponade due to effusion
  • raised cardiac enzymes
  • ECG- saddle shaped ST segment in all leads
102
Q

What may cause pericarditis?

A
  • autoimmune- SLE, RA, vasculitis, dresslers syndrome, sarcoidosis
  • malignancy
  • virus (EBV, CMV)
  • bacteria (lyme, TB, pneumonia)
  • trauma
  • uraemia
  • MI
103
Q

How should pericarditis be managed?

A
  • NSAIDS or aspirin for 2 weeks
    + colchine for 3 months
  • treat the cause (usually needs steroids)
104
Q

What features of bradycardia put someone at high risk of asystole? (so need intervention even when adverse signs not present)

A
  • recent asystole
  • mobitz type 2
  • complete/ 3rd degree heart block with broad qrs
  • ventricular pause <3s
105
Q

What drugs do all pts who have had an MI need to go home on?

A
  • clopidogrel 75mg - for 1 yr +/- PPI
  • bisoprolol 2.5mg od
  • aspirin 75mg- od (indefinate)
  • ramipril 5mg on
  • atorvastatin 80mg on
  • remember cardiac rehab and lifestyle advise also
106
Q

What is the cardioprotective diet

A

Reduce risk MI:

  • low refined sugar
  • low salt
  • ++ fibre
  • ++ unsalted fruit and nuts
  • whole grain
  • 2 portions fish a week
  • 5 portions fruit and veg a day
  • low fat intake (<30% kcal intake)

Y3 Medicine (9 decks)

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