Cardiology

Question 1

Screening age for AAA

Answer 1

65yr old male

Question 2

Causes of AAA

Answer 2

Obesity
Hypertension
Hyperlipidaemia
Smoking 
Connective tissue disorder

Question 3

Management of AAA

Answer 3

Treat underlying conditions

Indications for surgery:
Rupture
Symptomatic
>5.5cm or increasing >1cm per year

Question 4

ACEi side effects

Answer 4

Dry cough
Hyperkalaemia
First dose hypotension (expect upto 30% increase in serum creatinine and K+ of upto 5.5mM
Angioedema

Question 5

Two fates of a fatty plaque

Answer 5

Can narrow the CA and lead to reduced blood flow

Can rupture and a piece break off to occlude the artery

Question 6

ACS signs and symptoms

Answer 6

Central crushing chest pain radiating to the jaw and shoulders
Can be silent in diabetics or elderly

Also dyspnoea, sweating, N+V

Question 7

ACS investigations

Answer 7

ECG

Cardiac markers

Question 8

Management of ACS

Answer 8

Morphine
Oxygen (if <94%)
Nitrate
Aspirin (300mg)

Secondary prevention:
ACEi
Statin 
B-Blocker 
Aspirin
Second anitplatelet may be appropriate (clopidogrel) 

If present within 12hrs of symptoms and can deliver PCI within 120 mins then should deliver PCI (give praugrel if not on any other anticoagulants otherwise give clopidogrel- dual anti platelet therapy) otherwise fibrinolysis with an anti thrombin drug (give ticagrelor).

Question 9

Features of acute pericarditis

Answer 9

Sharp chest pain
Worse on inspiration
Relived on sitting forward 
Pericardial rub
Tachypnoea
Tachycardia

Question 10

Causes of pericarditis

Answer 10

Viral infection
Trauma 
Smoke inhalation
Hypothyroidism 
Malignancy
Connective tissue disorder
TB
Post MI

Question 11

Management of acute pericarditis

Answer 11

Rest and treat underlying cause

NSAIDs unless contraindicated then use colchicine

Question 12

Adenosine

Answer 12

Used to treat SVT
Should not be used in asthmatics (bronchospasms)
Leads to transient block of the AV node therefore reduces hyperpolarisation. Short t1/2 of 8 seconds therefore should be given via IV access

SE:
Bronchospasms
Chest pain
Transient flushing
Can enhance conduction of accessory pathways i.e. WPW syndrome

Question 13

Stable Angina

Answer 13

Treat with Aspirin, Statin and GTN spray.

First line treatment is either a CCB or BB.
If CCB (verapamil or diltiazem).
If not working then increase to max tolerated dose.
If not working then add either a CCB or BB, depending on which one you didn’t start with. In this case the CCB should be nifedipine.
If can’t handle dual therapy switch to mono therapy with long-acting nitrate, ivabradine etc

Question 14

Aortic dissection and RF

Answer 14

Tear in tunica intima

RF:
HTN
Collagen disease (Marfans, Ehlers-Danlos)
Turners syndrome
Pregnancy 
Bicuspid valve

Question 15

Aortic dissection features and classification

Answer 15

Features:
Severe chest pain, tearing and radiating to the back
Deficit in pulses (femoral, brachial, radial)
HTN
Specific arteries affected will have different effects; cardiac-angina, spinal-paraplegia, distal aorta- lower limb ischaemia

ECG non specific usually

Commonly Type A (2/3) ascending aorta
Type B (1/3) descending aorta

Question 16

Aortic dissection investigation and management

Answer 16

CXR- wide mediastinum 
CT angiography will show false lumen (conduct if pt stable)
Transoesophageal echo (if unstable pt)

Treatment:
Type A with surgery once stable BP of 100-120 systolic
Type B with conservative management, rest and anti-hypertensives

Complications of back tear- inferior MI, aortic incompetence
Complications of a front tear- unequal pulses/BP, renal failure, stroke

Question 17

Aortic regurgitation

Answer 17

Diastolic decrescendo murmur
+ve quinkes sign
Collapsing pulse

Causes include RF, biscuspid valve, collagen disorders, HTN

Question 18

Aortic stenosis

Answer 18

Murmur, dyspnoea, chest pain and syncope. Also slow rising pulse

Causes include senile calcification, bicuspid valve and post RF.

Monitor if asymptomatic, but if symptomatic or severe then need a valve replacement

Question 19

Types of AF

Answer 19

First onset
Paroxysmal- Self resolving within 24hrs-7 days
Persistent- Needs medical intervention, lasting greater than 7 days
Permanent- Cannot resolve with medical intervention.

NB- get dyspnoea, palpitations and chest pain.

Question 20

Treatment of AF

Answer 20

Rate control- In most cases.
Treat with CCB(diltiazem)/BB as a monotherapy or a dual therapy of CCB/BB/digoxin.

Rhythm controls- In cases of existing heart problems, first onset AF, easily reversible cause.
Treat with electrocardioversion if haemodynamically unstable. Otherwise treat with either electrical or pharmacological (amiodarone or fleiclanide if no structural heart problem)
NB if presents within 48hrs then no need for anticoagulants but if >48hrs need anticoagulants 3 weeks prior cardioversion.
Need to anticoagulants looks at CHADSVASc.

If giving warfarin look at HASBLED for bleeding risk >3 is increased risk.

Question 21

AF followed by stroke

Answer 21

Give warfarin or thrombin as choice of anticoagulation.

If no heamorrhage then anticoagulate after 2 weeks.

Question 22

Rate control catheter ablation

Answer 22

Can undergo ablation of the areas where extra signals are being sent.
Need to anticoagulate 4 weeks prior and follow on with lifelong anticoagulants to reduce the risk of stroke.

Complications include stroke, cardiac tamponade and pulmonary valve stenosis.

Question 23

Atrial flutter and management

Answer 23

SVT- Rapid depolarisation of the atria

Sawtooth appearance, can have a rate of 150bpm or greater depending on the ratio.

Treat same as AF; less responsive to the medication but very sensitive to the electro cardioversion, therefore lower energy levels required.
Can ablate the tricuspid valve isthmus as a cure

Question 24

Atrial myxoma

Answer 24

Most common form of primary cardiac cancer, commonly affecting the left atrium.

Dyspnoea, fatigue, weight loss, clubbing and pyrexia.
Also emboli, AF

Question 25

Atrial septal defects

Answer 25

Usually congenital defects found in adulthood with a high mortality rate. More commonly osteum secundum than osteum primum. Ejection systolic murmur, paradoxical embolism

Question 26

AV Block

Answer 26

1st degree- PR interval>20ms 2nd degree- Type 1- increasing PR until QRS drop Type2- constant PR with a random QRS drop 3rd degree- complete, no relationship between PR and QRS

Question 27

BNP

Answer 27

Made mainly by the left ventricle in response to strain, high levels can also indicate disorders of the LV Vasodilator Marker for HF- if low then unlikely HF=> use as first line diagnostic test Diuretic and natriuretic Suppresses sympathetic and RAAS pathway Increases with; LVH, ischaemia, tachycardia, sepsis, COPD, increased age, DM etc Decreases with obesity, diuretics, ACEi, BB, ARBs

Question 28

Cardiac enzymes and markers

Answer 28

Myoglobin is the first to rise Troponin will be a marker for MI but will be present for upto 10 days CK-MB is CK specific to the myocardium. Will resolve within a day therefore if still high can indicate a reinfarction

Question 29

Cardiac tamponade

Answer 29

Increased fluid build up and pressure in the pericardium Becks triad- Hypotension, increased JVP and muffled heart sounds Also get paroxysmal pulse (large BP drop on inspiration), dyspnoea, tachycardia absent Y-descent in JVP. Treat with immediate caridocentesis Get ECG electrical alternans- switching between tall and short QRS. In resitrictive pericarditis get present X and Y in JVP. No electoral alternans also

Question 30

Choking

Answer 30

Mild- Can speak Severe- Can’t speak, silent cough, wheezy etc Mild- encourage coughing Severe and conscious- 5 back blows, if unsuccessful then 5 abdominal thrusts, repeating this cycle until successful. Sever and unconscious- call for ambulance and start CPR.

Question 31

Clopidogrel

Answer 31

Indications- ischaemic stroke, PAD Less effective if used with PPIs

Question 32

Coarction of the aorta

Answer 32

Narrowing of the descending aorta, more common in males. Infancy-HF Adult- HTN Radiofemoral delay RF: Turners syndrome Bicuspid aortic valve Berry aneurysms

Question 33

Complete heart block

Answer 33

Syncope Wide pulse pressure HF Bradycardia

Question 34

Constrictive pericarditis

Answer 34

Same causes as acute pericarditis, more likely TB. Dyspnoea Increased JVP with X and Y present Signs of RSHF CXR will show pericardial calcification

Question 35

Dabigatran

Answer 35

Alternative AC to warfarin which doesn’t require any monitoring. Uses include prophylactic for DVT post TKR or THR. Also prophylaxis for stroke in non-valvular AF pts with CHADSVASc RF. Side effects include haemorrhage, dose should be altered in CKD patients. Reverse with idarucizumab

Question 36

DM- HTN

Answer 36

Should aim for BP <140/90 Use ACEi as renoprotective in DM Don’t use BB as they can increase insulin resistance, decrease secretion and impair autonomic response to hypoG.

Question 37

Dilated cardiomyopathy

Answer 37

``` Idiopathic During pregnancy HTN IHD Inherited- Duchennes muscular dystrophy ``` Leads to dilation of all four chambers, especially left ventricular- leads to predominantly poor systolic function

Question 38

ECG axial deviation

Answer 38

``` Left- LBBB WPWS- right accessory pathway Inferior MI hyperK ASD- osteum primum ``` ``` Right- RVH WPWS- left accessory pathway PE Cor pulmonale ASD- osteum secundum ```

Question 39

Bi/Tri fasicular block

Answer 39

Bifasicular- L/RBBB + hemiblock (axial deviation) Trifasicular- Bifasicular + heartblock NB LBBB- W in v1 M in v6 Causes include: IHD, HTN, aortic stenosis. If new then think ACS. RBBB- M in v1 W in v6 Causes include: normal variant, PE, MI RVH

Question 40

Digoxin ECG changes

Answer 40

ST depression- scooping Inverted/flattened T waves Short QT Arrhythmias

Question 41

ECG hypoK

Answer 41

U waves (after QRS) Small/absent, usually inverted T waves Long QT ST depression

Question 42

ECG hypothermia

Answer 42

J hump after QRS | Bradycardia

Question 43

ECG MI

Answer 43

Talk t waves first ST elevation Inverted T waves Pathological Q waves

Question 44

Atrial enlargement

Answer 44

Right- P wave increased height and amplitude Left- P wave increased amplitude and bifid

Question 45

ECG T-wave changes

Answer 45

Tall- hyperK and MI Inverted- MI, digoxin toxicity, PE, subarachnoid haemorrhage

Question 46

Acute HF Causes Investigations

Answer 46

Causes: Either de novo- less common, due to an increase in cardiac filling and pressure usually caused by an MI. Will lead to hypoperfusion and and pul oedema. Other causes of de novo include viral myopathy or toxins. Or decomprnsated HF- more likely, have a history of HF. Due to structural or functional changes caused by ACS, hypertensive crisis, valvular changes or acute arrhythmias. Investigations: Look for other causes- BT (anaemia? Electrolytes?), CXR (pul causes?), echo (valvular?) or BNP

Question 47

Acute HF treatment

Answer 47

``` O2 IV loop diuretics Opiates Vasodilators (nitrates) CPAP (sleep apnoea) ``` Consider discontinuing BB short term.

Question 48

Chronic HF Presentation Treatment

Answer 48

Presentation: Dyspnoea, orthopnoea, PND, cough (pink frothy sputum), bi basal lung crackles. RS- Raised JVP, hepatomegaly and leg oedema Treatment: Usually oral loop diuretics (furosemide) First line: ACEi or BB (bisoprolol) Second line: Aldosterone antagonist (spironolactone) Need to be wary of hyperK esp if used with ACEi Third line: Before starting need to refer to specialist. May initiate digoxin

Question 49

Heart sounds auscultation

Answer 49

P- Left sternal border, 2nd ICS A- Right sternal border 2nd ICS T- Left sternal border 4th ICS M-Left, medial to mid clavicular line, 5th ICS.

Question 50

Hypercalcaemia

Answer 50

Bones, stones, groans and psychic moans, thrones, tones. ``` Painful bones Renal stones Abdominal groans Psychic moans Thrones- Constipation/ frequent urination Tones- Muscle weakness, hyporeflexia ```

Question 51

Hypertension investigations

Answer 51

Usually asymptomatic unless very high BP in which case get seizures, headaches and visual disturbances Look for end organ damage: Fundoscopy Urine dipstick ECG Also: U+E HbA1C Lipids

Question 52

Management of hypertension

Answer 52

First line: <55yrs or T2DM- ACEi or ARB >55yrs or Afro-Caribbean (non T2DM)- CCB Second line: A+C or A+D (thiazide like diuretics) Third line: A+C+D After this: k+<4.5 spironolactone K+>4.5 a/B blockers Also consider lifestyle modifications, low salt diet

Question 53

Diagnosing hypertension

Answer 53

Most accurate to use 24hr BP monitoring, but use Home BP or ambulatory BP monitoring. >140/90 (clinic) then offer ABPM or HBPM: >135/85 - stage 1 hypertension- treat if <80yrs and has end organ failure, renal/CV disease, QRISK>10% >150/95- stage 2 hypertension- treat all cases

Question 54

HTN stages

Answer 54

Stage 1- 140/90 (clinic), 135/85 Stage 2- 160/100 (clinic) 150/95 Stage 3- >180 or />120

Question 55

Causes of HTN

Answer 55

Can be primary (unknown specific cause) Or secondary: Commonly primary hyperaldosteronsim Also Renal: GN, RAS, APKD, pyelonephritis Endocrine: Phaeochromocytoma (need to refer if suspecting this), primary hyperaldosteronism, Cushings, acromegaly Drugs: Steroids, NSAIDs, COCP Others: Pregnancy, coarction of the aorta

Question 56

Infective endocarditis

Answer 56

Think if fever and new murmur, usually affecting the mitral valve RF- previous episodes of IE, RF, prosthetic valves, IVDU (tricuspid affected mainly) Caused mainly by staph aureus, unless have in dwelling line or had prosthetic valve surgery Diagnose with 2 positive blood cultures showing organisms typical of infective endocarditis. Treat with flucloxacillin- effective against staph Give prophylaxis if previously infected pt develops an infection Surgery indicated if: not responding to Abx, severe valvular incompetence or aortic abscess

Question 57

Signs of inhaled foreign body

Answer 57

Cough Stridor Dyspnoea

Question 58

Palpitations

Answer 58

Causes include arrhythmias, anxiety or becoming more aware of heart beat. Tests- run an ECG, unlikely to see any changes in a few seconds so ask pt to take a Holter monitor (keeping a diary of when they felt palpitations and comparing to the rhythm strip) If this is not useful can consider an external/implantable loop recorder. Also do TFTs, U+Es (low K+), FBC

Question 59

Mitral regurgitation

Answer 59

Pansystolic murmur, radiating from the apex to the axils Usually asymptomatic but when more severe and get LVH then symptoms of HF Causes: RF, mitral valve prolapse, congenital, IE, post MI. ECG- may show atrial enlargement. CXR- may show caridomegaly. Diagnose with echo. Treatment- medical management if acute, repair is better than replacement. Replace in acute severe regurgitation.

Question 60

Mitral stenosis

Answer 60

Mid-late diastolic murmur heard better on expiration. Malar flush and AF. RHEUMATIC FEVER!!! CXR shows atrial enlargement Use echo.

Question 61

Complications of MI

Answer 61

``` Cardiac Arrest (following VF) Pericarditis Chronic HF Cardiogenic shock Left ventricular aneurysm VSD Tachyarrhthmias (VF) Bradyarrhythmias Acute mitral regurgitation ```

Question 62

Myocarditis

Answer 62

Suspect in young pt presenting with chest pain Look for cardiac enzymes, inflammatory markers and BNP Manage by treating underlying cause (Abx) and offering supportive treatment.

Question 63

Indications for temporary pacemaker

Answer 63

Trifasicular block before surgery Post anterior MI- type2 or complete heart block Symptomatic/haemodynamically unstable bradycardia

Question 64

Orthostatic hypotension

Answer 64

Drop in BP by 20/10 when standing Presyncope Syncope Treat with antihypotensives; flu for peristome or midodrine

Question 65

PE presentation

Answer 65

``` Dyspnoea Pleuritic chest pain Haemoptysis Tachypnoeic Tachycardic Usually resp examination unremarkable may hear some crackles ```

Question 66

PE investigations.

Answer 66

ECG- Sinus tachycardia, S1Q3T3 (s and a q large, t inverted- only on some cases find this pattern) Need to do the rule out criteria to rule out a PE If can’t rule out a PE then do the Wells score If >4 need to do a CTPA, give DOACs whilst waiting for the diagnosis confirmation. If +ve then continue DOAC treatment, if -ve then conduct a proximal leg vein ultrasound if DVT suspected. If <4 then do a d-dimer, if +ve then do CTPA and give DOACs whilst waiting for diagnosis. If this comes back -ve then stop DOACs.

Question 67

PE management

Answer 67

Prescribe DOACs unless they have me severe renal impairment or APLS in which case give LWMH followed by Vit-K antagonist (Warfarin) PE can either be provoked or unprovoked. Provoked- Give DOACs for 3 months total Unprovoked- Give DOACs for 6 months total- whilst monitoring the HASBLED risk. If massive PE/haemodynamically unstable then consider thrombolysis as first line treatment.

Question 68

Rheumatic Fever

Answer 68

Immunological reaction to a strep pyogenes infection (within 2-6 weeks) ``` +ve throat swap Erythema marginatum Polyarthritis Pyrexia Raised CRP/ESR ``` Management: Oral penicillin NSAIDs

Question 69

Statins

Answer 69

ADR- myalgia, rhabdomyolysis, liver impairment. Contraindicated in pregnancy and with macrolides. Uses: Established CV event (Stroke, TIA, AF, PAD, ACS) QRISK>10% DM for over 10 years, over the age of 40yrs or with established nephropathy. Primary prevention: Atorvastatin 20mg Secondary prevention: Atorvastatin 80mg

Question 70

SVT

Answer 70

Acute management: Valsalva manoeuvre IV Adeonsine (6mg->12mg->12mg) Electrical cardioversion Prevention: B-blockers Radio frequency ablation

Question 71

Syncope

Answer 71

This is the transient loss of consciousness with a rapid onset, short duration and full spontaneous recovery. Reflex: (most common) Vasovagal- emotions, ‘fainting’, stress, pain Situational- cough, micturition Carotid sinus syncope Orthostatic: Primary autonomic- Parkinsonism, LB dementia Secondary autonomic- DM nephropathy Cardiac: Arrhythmias Structural- valves, MI Other- PE Look at postural drop in BP

Question 72

Thiazide diuretics ADR

Answer 72

``` Dehydration HypoK/Na HyperCa Gout Impotence Impaired glucose tolerance ```

Question 73

Takayasu’s arteritis

Answer 73

``` Vascular is of the large vessel, common in Asian and female. Occlusion of the aorta: Absent limb pulses Intermittent claudication Difference in BP across upper limbs Carotid bruit ``` Manage with steroids

Question 74

Thrombolysis

Answer 74

Give to convert plasminogen into plasmid therefore leading to fibrin breakdown. Alteplase, streptokinase Risk of bleeding and hypotension

Question 75

Tricuspid regurgitation

Answer 75

Pan systolic murmur Pulsation hepatomegaly Left parasternal heave ``` Causes: RV infarction Rheumatic heart disease Infective endocarditis Pulmonary hypertension (COPD) ```

Question 76

VSD

Answer 76

More common with chromosomal disorders I.e. Downs, Edwards Congenital infections Or acquired I.e. post MI VSD may be small and asymptomatic in which case they close spontaneously. Can also be larger and symptomatic- Require treatment (present with HF), nutritional support and surgical repair. Post natal presentation: Failure to thrive, HF symptoms, pan systolic murmur. Complications: Aortic regurgitation, infective endocarditis, RSHF, pulmonary hypertension

Question 77

Ventricular tachycardia

Answer 77

Can be monomorphic- common, post MI. Or polymorphic- I.e. Torsades de pointes (VT with long QT) Need to treat since can progress to VF and then cardiac arrest. Management: If signs of haemodynamic instability present then need elctorcardioversion. If not present then medical treatment; amiodarone (central line) or lidocaine. If not responding then synchronised cardioversion. Do not use VERAPAMIL If drug therapy does not work then may need implanted defibrillator

Question 78

Warfarin

Answer 78

Inhibits the conversion of Vitamin K therefore reduces clotting Used in VTE target INR<2.5, 3.5 for recurrent episodes Used in AF target INR<2.5 Also used in mechanical heat valves Potentiated by liver disease, P450 inhibitors, drugs displacing warfarin from albumin (NSAIDs), cranberry juice

Question 79

Bleeding risk with Warfarin

Answer 79

Anything INR>5 need to consider stopping warfarin and giving Vitamin K. Greater INR- greater bleeding risk

Question 80

WPWS

Answer 80

Congenital accessory pathway between the atria and the ventricles, if not treated then the AF can develop quickly into VF. ECG: Short PR Axis deviation Wide QRS with delta wave (upstroke) Treat with radio frequency ablation of the accessory pathway. Medical- sotalol (avoid in coexisting AF), amiodarone or flecainide.