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3rd yr clinical > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the primary prevention for CVD?

A

Meds based on QRISK3 - if over 10% give statin or if patient has CKD/T1D

20mg atorvastatin
Aim for 40% reduction in lipids after 3 months

statins interact with macrolide antibiotics eg. clarith

Can cause muscle weakness

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2
Q

What are the medications given for secondary prevention of CVD

A

6A’s

Antiplatelet- Aspirin + Clopidogrel
Atorvastatin (80mg)
Atenolol (or other beta blocker- max dose)
Ace inhibitors (ramipril - max dose)

If HF give an aldosterone antagonist - spironolactone

Ace inhibit + spironolactone together cause high risk of K+

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3
Q

What anti platelet therapy will a patient get after an MI?

A

For 12 months they will get dual anti-platelet therapy along with the other 4A’s

Aspirin 75mg and Clopidogrel for 12 months

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4
Q

What are the treatment options for stable angina

A

Immediate relief- GTN sublingual spray

Long term relief- Beta-blocker, calcium channel blocker (avoid in HF with reduced EF)

Surgical intervention
PCI- balloon and stent insertion
CABG- bypass

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5
Q

What ECG changes can be seen in an MI

A

STEMI- ST elevation and new LBBB

NSTEMI- ST segment depression/ no change and T wave inversion

If an NSTEMI- use troponin to diagnose

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6
Q

What ECG leads will show changes for a blockage in the

LCA
LAD
Circumflex
RCA

A

LCA- I, aVL, V3-6 - anterolateral (bigger numbers, bigger blood supply)

LAD- V1-4 (4 lads)

Circumflex- I, AVL, V5-6 (Not LAD but still left)

RCA- II,III,aVF (weird ones)

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7
Q

What is the initial management of an MI

A

MONA
Morphine (IV) with antiemetic
Oxygen
Nitrates (GTN)
Aspirin 300mg

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8
Q

What are the options for hospital management of a STEMI

A

PCI- if patient gets to hospital within 2 hrs of presentation

Thrombolysis- fibrinolytic agent like streptokinase * significant bleeding risk*

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9
Q

What is the initial management of an NSTEMI

A

BATMAN

-base decision about angiography/PCI
-Aspirin 300mg stat
-Ticagrelor 180mg stat (clopidogrel if high risk of bleeding)
-Morphine
-Anti-thrombin therapy
-nitrate

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10
Q

What is Dressler’s syndrome?

A

Post MI syndrome 2-3 weeks after- inflammation of pericardium
-Pleuritic chest pain, low grade fever and pericardial rub
-ECG- global ST elevation and T wave inversion

Management
NSAIDs, steroids, percardiocentesis

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11
Q

What are the causes, presentation and management of pericarditis ?

A

Causes
Infection, autoimmune injury, uraemia, methotrexate, cancer

Presentation
Sharp chest pain (pleuritic), worse lying down, better sitting forward

Management
NSAIDs
Colchichine (for 3 months)

Second line- steroids

Treat underlying cause

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12
Q

What is the cause of LVHF and what are the main investigations

A

Reduced CO causes a backlog of blood in the in left atrium and pulmonary vessels - fluid leaks into lungs- pulmonary oedema

Will hear 3rd HS and bibasal crackles on auscultation

BNP most important in bloods
ECHO to measure LV function - over 50% is normal
CXR- - cardiomegaly and upper lobe diversion– pressure in back veins

Management
Diuretics
Sit up
Stop IV fluids
Monitor fluid balance

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13
Q

What are the causes of chronic HF and how is it managed

A

-IHD, Valve disease (aortic stenosis), HTN, Arrhythmias, cardiomyopathy

Medical treatment-ABAL
Ace inhibitor - in valve disease give an ARB instead (candesartan)
Beta blocker
Aldosterone antagonist- spironolactone
Loop directive

Other specialist meds-
SGLT2 inhibitor
Digoxin

Surgical management
Implantable cardioverter defibrillator if patient has had ventricular tachycardia/ fib

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14
Q

What must be monitored when on medication for HF

A

U&E
Ace inhibitors and aldosterone antagonists both can cause hyperkalaemia

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15
Q

What investigations are done in a patient with newly diagnosed HTN?

A

Urine albumin creatine ratio Urine dipstick for proteinuria and haematuria
Bloods- HbA1c, u&E, lipids
Fundus exam
ECG

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16
Q

What is the management for hypertension in patients under 55

A

Ace inhibitors- rampapril
Beta blocker

Depending on serum potassium Thiazide diuretic (indapamide)

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17
Q

What is the management for HTN in patients over 55

A

CCB (amlodipine)
Beta blocker
Thiazide diuretic

18
Q

What is the management for HTN in afrocarribean patients

A

CCB (amlodipine)
beta blocker
Thiazide diuretic

19
Q

How do diuretics affect serum potassium

A

Thiazide diuretics can cause hypokalaemia due to increased excretion of potassium

If this occurs you can use a potassium sparing diuretic like spironolactone which causes sodium and water excretion but potassium reabsorption

20
Q

What are the causes and presentation of aortic stenosis

A

Age related calcification
Bicuspid aortic valve
Rheumatoid HD

Ejection systolic high pitched crescendo decrescendo murmur
Radiates to carotids
Thrill in aortic area
Slow rising pulse
Narrow pulse pressure
Exertional syncope

21
Q

What are the causes and features of aortic regurgitation

A

Age related weakness
Bicuspid aortic valve
Connective tissue disorders- Marfans sydrome

Early diastolic murmur - rumbling
Thrill in aortic area
Collapsing pulse
Wide pulse pressure
HF and pul oedema (back pressure into LV)

22
Q

What are the causes and features of mitral stenosis

A

Rheumatic HD
Infective endocarditis - splinter haemorrhages, janeway lesions, osler’s nodes

Mid- diastolic low pitched rumbling
Tapping apex beat
Malar flush- back pressure on pulmonary system
Atrial fibrillation

23
Q

What are the main features and causes of mitral regurgitation

A

Weakening of valve with age
IHD
Infective endocarditis
Rheumatic HD
CT disorders

Pansystolic high pitches whistling
Radiates to left axilla
Thrill on mitral area
Signs of HF and pul oedema
Atrial fibrillation

24
Q

What are the risk factors and bacterial causes of infective endocarditis

A

IV drug use, Structural heart pathology, CKD, immunocompromised, history

Causes
Staphylococcus - staph aureus
Streptococcus (viridian’s group)
Enterococcus (faecalis)

25
Q

What is the presentation and investigations for infective endocarditis

A

-fever, fatigue, night sweats muscle aches, anorexia, new murmur, splinter haemorrhages, petechiae (non blanching red spots), laneway lesions , oilers nodes (both on pads of fingers)

Do blood cultures before abx
Cultures separated by at least 6 hrs and taken from different sites

Transoesophageal echo - better than transthoracic

Vegetation seen on valves

26
Q

How is infective endocarditis diagnosed

A

The modified duke criteria
Requires one major and 3 minor criteria or 5 minor criteria

Major
Positive blood cultures
Imaging findings (vegetations)

Minor
Risk factors
Fever over 38
Vascular phenomena (laneway lesions, ICH, splenic infarct)
Immunological phenomena (oslers nodes, glomerulonephritis)
Microbiological phenomena (positive cultures)

27
Q

What is the management of infective endocarditis

A

IV antibiotics - amoxicillin and gentamicin for at least
4 weeks if valves are natural
6 weeks if prosthetic

28
Q

What is the presentation and management of hypertrophic obstructive cardiomyopathy

A

SOB, fatigue, dizzy, syncope, chest pain, palms

Ejection systolic murmur at lower left sternal border (louder on valsalva manoeuvre), fourth HS and thrill over left sternal border

Management
Genetic testing, ECG,CXR, Echo

Beta blockers
Surgical myectomy
Septal ablation
Implantable cardioverter defibrillator

Avoid intense exercise, dehydration, ACE inhibit and nitrates

29
Q

What are the main causes and investigations in AF

A

SMITH
Sepsis, mitral valve pathology, ischaemic HD, thyrotoxicosis, HTN

ECG- absent p waves, narrow QRS complex tacky, irregularly irreg rhythm
Echo to investigated causes
CHA2DVASc score to work out need to anti-coat

30
Q

What are the management steps in AF

A
  1. Rate control - beta blocker 1st line then CCB or digoxin
  2. Rhythm control using cardio version- flecanide or amiodarone/ electrical

or long term medication (beta blockers 1st line then amiodarone)

  1. Anticoagulation - DOACs first line (apixaban)
    then warfarin

4.Assess CHA2DS2VASc score and ORBIT bleeding score

31
Q

How do you choose between immediate and delayed cardio version

A

Immediate cardioversion- choose if AF is present for less than 48 hrs or they are life threateningly haemodynamically unstable
Done with flecanide/ amiodarone or electrical

Delayed cardio version- if AF present for more than 48 hrs and patient is stable
Done using transoesophageal echocardiography guided cardioversion

In delayed - patients should be anticoagulated for 3 weeks with rate control before

32
Q

What is Wolff- Parkinson White syndrome

A

A type of supra ventricular tachycardia
An extra-electrical accessory pathway

cannot give anti-arrhythmic medications in people with this condition- like beta blockers etc - this can reduce AV conduction and will end up promoting accessory pathway conduction

Radiofrequency ablation of the accessory pathway is the treatment

33
Q

What is the stepwise management of SVT

A
  1. Vagal manoeuvres
    Valsalva- blow into syringe
    Carotid massage
    Diving reflex- submerge face in cold water
  2. Adenosine
    (A DOWN o sine) - rapid IV bolus into a large cannula 6mg, 12mg, 18mg
    Feeling of impending doom

3.Verapamil/beta blocker

  1. DC cardioversion
34
Q

Which cardiac arrest arrhythmia are shockable and non shockable

A

Shockable: Ventricular tachycardia, ventricular fibrillation

Non shockable: systole, pulseless electrical activity

35
Q

What is atrial flutter

A

Atrial rate around 300bpm
signal doesn’t reach ventricles every time
Sawtooth on ECG
Same treatment to AF- anticoagulant and radio frequency ablation

36
Q

What are the causes and management of QT prolongation

A

Causes
Long QT syndrome
Antipsychotics, citalopram. flecnidine, amiodarone, macrolide antibiotics
Hyperkalaemia, hypocalcaemia

Torsades de pointes - associated with subarachnoid haemorrhage, will either stop or go to ventricular tachycardia
Give a magnesium infusion to manage, or defibrillator

Management
Stop meds causing it
Correct electrolytes
Beta blockers
Implantable cardioverters

37
Q

What is first degree heart block

A

Every atrial impulse leads to a ventricular contraction just a longer PR interval >0.5

38
Q

What is mobitz type 1 (Wenckebach) heart block

A

Conduction through AV node gets longer every time and then doesn’t appear and then repeats

Increasing PR interval until a p wave isn’t followed by a QRS

39
Q

What is mobitz type 2 heart block

A

Set ratio of P waves to QRS complexes

40
Q

What is third degree heart block

A

No relationship between P and Q waves

41
Q
A

3rd yr clinical (22 decks)

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