Cardiology

Question 1

central, pleuritic chest pain and fever 4 weeks following a myocardial infarction suggests what?

Answer 1

Dresslers - Pericarditis following MI

Question 2

traumatic accident with respiratory distress, hypotension, jugular venous distension, and absent lung sounds suggests what?

Answer 2

Tension pneumothorax

Question 3

A third heart sound is considered normal
in patients under what age?

Answer 3

<30 years old

Question 4

What are the common causative organisms of infective endocarditis?

Answer 4

Most common/IVDU - Staph aureus
Those with poor dental hygiene/post dental proceudure - Strep viridans
Following prosthetic valve surgery - Staph epidermidis

Question 5

Widened mediastinum on CXR with severe chest pain suggests what?

Answer 5

Aortic dissection

Question 6

In ALS, if IV drugs cannot be given, how should they be given?

Answer 6

Intraosseous

Question 7

What is the most specific ECG finding in acute pericarditis?

Answer 7

PR depression

Question 8

Type A (ascending) vs Type B (descending) aortic dissection?

Answer 8

A - chest pain
B - upper back pain

Question 9

tall R waves in leads V1-3 are a classic finding for what?

Answer 9

Posterior MI

Question 10

What score should be used to assess the risk of bleeding when starting someone on anticoagulation in AF?

Answer 10

Orbit

Question 11

What are reversible causes of cardiac arrest?

Answer 11

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins

Question 12

When should warfarin be stopped prior to surgery?

Answer 12

5 days before

Question 13

What is the key diagnostic finding of aortic dissection on CT?

Answer 13

False lumen

Question 14

What are C/I to thrombolysis?

Answer 14

active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension

Question 15

weak or absent carotid, brachial, or femoral pulse
variation in arm BP suggests what?

Answer 15

Aortic dissection

Question 16

When can electrical cardioversion be considered for patients with AF?

Answer 16

If presenting within 48 hours

Question 17

What medication should be stopped when patients are given a course of macrolides e.g. clarithromycin?

Answer 17

Statins

Question 18

Thiazide-like diuretics should not be used in patients with what?

Answer 18

Gout

Question 19

ST elevation and acute pulmonary oedema in a young patient with a recent flu-like illness suggests what?

Answer 19

Myocarditis

Question 20

When should rhythm control be used for AF instead of rate control?

Answer 20

coexistent heart failure, first onset AF or an obvious reversible cause

Question 21

Which medication can reduce hypoglycaemia awareness?

Answer 21

Beta blockers

Question 22

Which medication can impair glucose tolerance?

Answer 22

Thiazides

Question 23

Widespread ST elevation in V1-4 suggests what?

Answer 23

100% occlusion of the LAD

Question 24

Erythromycin can cause which cardiac abnormality?

Answer 24

QT prolongation

Question 25

What kind of bacteria is staph aureus?

Answer 25

Gram positive cocci

Question 26

How should a patient with minor bleeding with INR > 8 be managed?

Answer 26

Stop warfarin and give IV Vitamin K with repeat dose of Vit K after 24 hours if INR still high

Question 27

What drugs can cause hypokalaemia?

Answer 27

Loop diuretics e.g. furosemide

Question 28

A new left bundle branch block should raise alarms for what?

Answer 28

ACS

Question 29

What scoring system should be used to identify patients with a pulmonary embolism that can be managed as outpatients?

Answer 29

Pulmonary Embolism Severity Index (PESI)

Question 30

How does fondaparinux work?

Answer 30

Activates antithrombin III

Question 31

What is the management of AF if ChadsVasc is 0?

Answer 31

Echo to rule out valvular causes

Question 32

What are ecg findings of hypokalaemia?

Answer 32

small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
U waves

Question 33

What is the second-line therapy in patients with HFrEF?

Answer 33

SGLT-2 inhibitors e.g Empagliflozin

Question 34

inferior myocardial infarction and AR murmur suggests what?

Answer 34

Proximal aortic dissection

Question 35

High dose statins should be commenced in stroke patients when?

Answer 35

48 hours after stroke

Question 36

What criteria should be used for infective endocarditis?

Answer 36

Duke criteria

Question 37

What criteria should be used for rheumatic fever?

Answer 37

Jones criteria

Question 38

What drugs should be used for anticoagulation in those with mechanical heart valves?

Answer 38

Warfarin/LMWH

Question 39

Complete heart block following an MI suggests the lesion is where?

Answer 39

Right coronary

Question 40

Investigation of choice for aortic dissection?

Answer 40

CT Angio

Question 41

Management of aortic dissection

Answer 41

Control BP with IV Labetalol and surgery

Question 42

Most common ECG change of PE?

Answer 42

Sinus tachycardia

Question 43

CP of pericarditis?

Answer 43

• pleuritic chest pain: worsen lying flat and relieved by sitting forward
• fever
• pericardial rub
• tachycardia and tachypnea
• non-productive cough
• dyspnoea
• flu-like symptoms

Question 44

What may a pericardial rub indicate? (friction of heart against pericardium, sounds like sandpaper rubbed on wood)

Answer 44

pericarditis

Question 45

Ix for pericarditis?

Answer 45

• all pts with suspected= TRANSTHORACIC ECHO
• ECG
• bloods: inflam markers, only 30% have elevated troponin

Question 46

Pericarditis is associated with what?

Answer 46

pericardial effusion that can sometimes worsen to cardiac tamponade

Question 46

ECG findings for pericarditis?

Answer 46

• PR depression
• ‘saddle-shaped’ ST elevation

PeRicardiTiS

Question 47

Management of pericarditis?

Answer 47

NSAIDs plus colchicine

Until CP resolution and normal inflam markers (usually 1-2w) followed by tapering of dose recommended

Question 48

PR Depression on ECG is indicative of what?

Answer 48

Pericarditis

Question 49

Medical management of NSTEMI?

Answer 49

dual antiplatelet therapy, an ace inhibitor, a beta-blocker, and a statin

Question 50

What is Beck’s triad?

Answer 50

• Raised JVP
• Muffled heart sounds
• Falling BP

Question 51

What is Beck’s triad a sign of?

Answer 51

Cardiac tamponade

Question 52

Management of major bleed with someone on warfarin?

Answer 52

stop warfarin, give intravenous vitamin K 5mg, prothrombin complex concentrate

Question 53

How should episodic palpitations be investigated?

Answer 53

Holter monitoring

Question 54

notching of the inferior border of the ribs suggests what?

Answer 54

Aortic coarctation

Question 55

Management of PE with low PESI score?

Answer 55

Can be managed as an outpatient with DOAC

Question 56

Nitrates for MI are contraindicated when?

Answer 56

Patients with hypotension

Question 57

What is the treatment for torsades de pointes?

Answer 57

IV Mag Sulph

Question 58

What is a normal cardiac variant in athletes?

Answer 58

First degree heart block

Question 59

Investigation of choice for someone with PE and renal impairment?

Answer 59

V/Q scan

Question 60

What is normal in an athlete and does not require any intervention?

Answer 60

First degree heart block

Question 61

If angina is not controlled by a beta blocker, what should be added?

Answer 61

Amlodipine

Question 62

What should be used if atropine if not helping with bradycardia?

Answer 62

• transcutaenous pacing
• transvenous pacing

Question 63

Sydenham’s chorea is a complication of what?

Answer 63

Rheumatic fever

Question 64

Management of persistent myocardial ischaemia following fibrinolysis

Answer 64

PCI even if time elapsed

Question 65

What on echo is used to determine the severity of aortic stenosis?

Answer 65

Trans-valvular pressure gradient

Question 66

What is Buerger’s disease?

Answer 66

aka thromboangiitis obliterans

• A small/medium vasculitis which is associated with smoking
• CP: intermittent claudication, Raynaud’s, ischaemic ulcers, superficial thrombophelbitis

Question 67

What is the mode of action of statins?

Answer 67

Decrease intrinsic cholesterol synthesis by inhibiting HMG-CoA reductase enzyme

Question 68

How to manage a strong suspicion of PE whilst waiting for scan?

Answer 68

Start treatment dose anticoagulant

Question 69

Electrical alternans is a sign of what?

Answer 69

Cardiac tamponade

Question 70

J waves are associated with what?

Answer 70

Hypothermia

Question 71

Hypertrophic obstructive cardiomyopathy is associated with what?

Answer 71

Wolf-Parkinson-White

Question 72

Management of acute heart failure not responding to furosemide?

Answer 72

Consider CPAP

Question 73

What is a complication of MI?

Answer 73

Pulmonary oedema

Question 74

SVT Management?

Answer 74

1. Valsalva
2. IV Adenosine upto 3 doses
3. Electrical cardioversion

Question 75

Criteria for rate control vs anticoag/cardioversion?

Answer 75

• Under 65
• No Hx of IHD

Question 76

Thrombus in aVL, which artery?

Answer 76

Left circumflex

Question 77

What is Framingham risk score?

Answer 77

estimate the 10-year risk of heart attack

Question 78

severe hypertension and bilateral retinal hemorrhages and exudates

Answer 78

Malignant HTN

Question 79

Endocarditis - which valves are affected?

Answer 79

Mitral - most common
Aortic
Tricuspid - IVDU

Question 80

A patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination

Answer 80

VSD

Question 81

Treatment for cardiac tamponade?

Answer 81

Urgent pericardiocentesis: Pericardial needle aspiration

Question 82

What is Kussmaul sign?

Answer 82

• JVP rises on inspiration
• Sign of constrictive pericarditis

Question 83

holosystolic murmur, high-pitched and ‘blowing’ in character

Answer 83

Mitral regurg

Question 84

Tachycardia and tachypnoea with no signs

Answer 84

Think PE

Question 85

Can warfarin be used when breast feeding?

Answer 85

Yes

Question 86

What electrolyte abnormality do thiazide diuretics cause?

Answer 86

• Hypokalaemia
• Hyponatraemia
• Hypercalcaemia
• Gout
• Impaired glucose tolerance

Question 87

Management of irregular broad complex tachycardia

Answer 87

Seek cardiology input

Question 88

What is Takayasu’s arteritis?

Answer 88

• Systemic features of vasculitis
• Unequal BP in upper limbs
• Carotid tenderness
• Absent/weak peripheral pulses
• Associated with renal artery stenosis
• MRA/CTA to treat with steroids

Question 89

Low pitched diastolic murmur?

Answer 89

Mitral stenosis

Question 90

Acute mitral valve regurg + pulmonary oedema

Answer 90

Think MI

Question 91

What is the dose of adrenaline used in cardiac arrest?

Answer 91

1mg of IV adrenaline

Question 92

Breathing problems with clear chest

Answer 92

PE

Question 93

What is Brugada syndrome?

Answer 93

• AD disorder which can cause sudden death
• autosomal dominant; more common in Asians
• can be caused by mutation in SCN5A gene (encodes for myocardial sodium ion channel protein)
• ECG shows ST elevation and T wave inversion (may become clearer after giving flecainide- Ix of choice)
• Mx is implantable cardioverter-defib

Question 94

Most common place of inhaled foreign body?

Answer 94

Right inferior bronchus

Question 95

Findings for aortic stenosis?

Answer 95

narrow pulse pressure
slow rising pulse
a thrill palpable over the cardiac apex
a fourth heart sound (S4) indicative of left ventricular hypertrophy
a soft/absent S2

Question 96

Which medications can cause torsades de pointes?

Answer 96

Macrolides e.g. azithromycin

Question 97

What condition are ACE inhibitors C/I with?

Answer 97

Renovascular disease

Question 98

What causes the acute mitral regurg following MI?

Answer 98

Rupture of the papillary muscle/ischaemia

Question 99

When can you commence spironolactone for HTN?

Answer 99

When already taking ACE, CCB and thiazide-like diuretic + K is below 4.5

Question 100

When should adrenaline be given for shockable rhythms?

Answer 100

After 3 unsuccessful shocks

Question 101

Pericarditis vs Myocarditis?

Answer 101

Myocarditis -> elevated troponin

Question 102

Which markers can you test for STEMI?

Answer 102

Troponin, CK, AST, LDH

Question 103

What ECG changes might be seen following STEMI?

Answer 103

T wave inversion, pathological Q waves

Question 104

Driving rules post MI

Answer 104

• No need to inform DVLA
• Can drive after1 week if successful angioplasty
• Can drive after 4 weeks if no angio/unsuccessful angio

Question 105

Complication of coronary angio

Answer 105

Bleeding, haemorrhage, infection, MI, stroke, damage to coronary vessels, death

Question 106

What triggers are there for angina?

Answer 106

Exertion, cold weather, emotions such as anger, vivid dreams

Question 107

How does aspirin work?

Answer 107

Inhibits COX which inhibit thromboxane which inhibits platelets aggregation

Question 108

Abnormally large drop in BP during inspiration?

Answer 108

Pulsus paradoxus -> Cardiac tamponade

Question 109

How should diabetes be managed following MI?

Answer 109

Use IV insulin infusion and stop the oral diabetes meds

Question 110

patients with a GRACE score > 3% should have what?

Answer 110

Coronary angio within 72 hours

Question 111

Management of persistent MI following fibrinolysis

Answer 111

PCI

Question 112

What is the treatment of broad complex tachycardias?

Answer 112

• Amiodarone

Question 113

Single episode of paroxysmal AF?

Answer 113

ChadsVasc and consider DOAC

Question 114

Management of IE causing congestive cardiac failure

Answer 114

Emergency valve replacement

Question 115

What is the alternative to 3 weeks of anticoagulation for someone having cardioversion with AF?

Answer 115

Transoeseophageal echo to exclude left atrial appendage thrombus

Question 116

What are warfarin INR targets for mechanical valves?

Answer 116

Aortic - 3.0
Mitral - 3.5

Question 117

What is the NYHA heart failure classification?

Answer 117

Class 1 - no symptoms and no limitations
Class 2 - mild symptoms with slight limitation (some fatigue, dyspnoea)
Class 3 - moderate symptoms with marked reduction in activity (symptoms anytime except rest)
Class 4 - severe symptoms and symptoms of HF present even at rest

Question 118

When is AAA screening done?

Answer 118

Men aged 65

Question 119

How is AAA screening managed?

Answer 119

< 3 cm - normal
3 - 4.44cm - rescan every 12 months
4.45 - 5.4cm - rescan every 3 months
>5.5 - refer to vascular surgery within 2 weeks

Other referral criteria
- Rapidly growing (>1cm per year)

Question 120

What is the biggest indicator of a poor prognosis in someone with MI?

Answer 120

Cardiogenic shock

Question 121

What would an ABG for pulmonary embolism show?

Answer 121

Respiratory alkalosis -> hyperventilation

Question 122

When is staph epidermidis the most common organism causing endocarditis?

Answer 122

If <2 months post valve surgery

Question 123

Why is verapamil C/I in heart failure + VT?

Answer 123

It can slow down contractility of the heart even further

Question 124

What is the most common cause of death in patients post MI?

Answer 124

V Fib

Question 125

Haemoptysis can be a symptom of what?

Answer 125

Mitral stenosis

Question 126

mid-diastolic low-pitched rumbling murmur

Answer 126

mitral stenosis

Question 127

Management of BP > 180/120 in GP

Answer 127

If unstable/signs of papilloedema/retinal haemorrhages -> refer to specialist
If stable then arrange urgent investigations for organ damage eg. bloods, urine ACR, ECG

Question 128

What is the normal QRS value?

Answer 128

<0.12s / 3 small squares

Question 129

What are signs of left ventricular failure?

Answer 129

Dyspnoea, reduced exercise tolerance, fatigue, paroxysmal nocturnal dyspnoea, orthopnoea, wheeze, cough (worse at night), pink, frothy sputum

Question 130

What are signs of right ventricular failure?

Answer 130

Peripheral oedema, facial engorgement and abdominal distension

Question 131

What are causes of AF?

Answer 131

Pneumonia, MI, PE, Alcohol excess, HF, Endocarditis

Question 132

What are signs of aortic regurg?

Answer 132

• Collapsing pulse
• Early diastolic murmur
• Wide pulse pressure
• Displaced apex
• Carotid pulsation: Corrigans sign
• pulsation of nail bed: Quincke’s sign

Question 133

Absent arm pulses in a young woman?

Answer 133

Think Takayasu’s arteritis

Question 134

AF + mass in left atrium

Answer 134

Cardiac myxoma - bengin tumour of the heart

Question 135

Patients with aortic valve IE are at risk of what?

Answer 135

Developing aortic valve abscess (prolongation of PR can be first sign)

Question 136

What pulse can you get with heart failure?

Answer 136

Pulsus alternans - strong and weak beats due to varying systolic pressure

Question 137

When is rhythm control used in AF treatment over rate control?

Answer 137

• Coexistent HF
• First onset AF
• Obvious reversible cause
• Use amiodarone/flecainide

Question 138

What is the inheritance of HOCM?

Answer 138

AD

Question 139

What is the pathophysiology of HOCM?

Answer 139

• Diastolic dysfunction as LVH causes decreases compliance and decreased CO
• Biopsy shows myofibrillar hypertrophy with disarrayed myocytes

Question 140

ECG findings for hypercalcaemia?

Answer 140

Short QT

Question 141

What are the components for JONES criteria?

Answer 141

Joint involvement
<3 - Myocarditis
Nodules
Erythema marginatum
Sydnehams chorea

Question 142

Post MI patient develops pulmonary oedema and has pansystolic murmur?

Answer 142

Think acute mitral regurg

Question 143

What can cause orthostatic hypotension?

Answer 143

• Excercise induced
• After meals
• After prolonged bed rest
• Drugs such as CBB, Levodopa

Question 144

QT prolongation with no electrolyte abnormalities?

Answer 144

Think hereditary long QT syndrome -> caused by loss of function/blockage of K+ channels

Question 145

When should LFTs be checked with statins?

Answer 145

Baseline, 3 months and 12 months

Question 146

What murmur do you get with VSD?

Answer 146

Pansystolic murmur - entire systolic period

Question 147

Which drug when used alongside clopidogrel can make it less effective?

Answer 147

Omeprazole/Esomeprazole

Question 148

What dose of amiodarone is given in ALS?

Answer 148

Initially 300mg
After 5th shock, an additional 150mg can be given alongside 1mg of adrenaline

Question 149

What will type A aortic dissection cause?

Answer 149

Acute aortic regurg

Question 150

What is the treatment for rheumatic fever?

Answer 150

IM BenPen or Oral PenV with NSAIDs

Question 151

Patients taking isosorbide mononitrate should use what dosing regime?

Answer 151

Asymmetric dosing interval to prevent nitrate tolerance

Question 152

NSTEMI in an unstable patient?

Answer 152

Immediate coronary angio

Question 153

Which antihypertensive cause hyperkalaemia?

Answer 153

ACE

Question 154

What is tongue and facial swelling?

Answer 154

Angioedema -> ACE inhibitor

Question 155

What are examination signs of pericarditis?

Answer 155

-Pericardial rub
- Quiet heart sounds
- Raised JVP

Question 156

What are causes of pericarditis?

Answer 156

• Infective: coxsackie, TB
• Trauma
• Malignancy eg. lung/breast
• MI complication
• SLE
• RA
• hypothyroidism

Question 157

3 main investigations for IE?

Answer 157

• Blood cultures
• Echo
• ECG

Question 158

What are some triggers for worsening pulmonary oedema?

Answer 158

• Arrhythmia
• MI
• Sepsis

Question 159

What is the most common cardiomyopathy?

Answer 159

Dilated

Question 160

management of mitral stenosis?

Answer 160

Asymptomatic - Monitor with regular echo
Symptomatic - Percutaneous mitral commissurotomy

Question 161

When fibrinolysis is done for ACS, when should ECG be repeated?

Answer 161

60-90 minutes

Question 162

What are the ChadsVasc categories?

Answer 162

Congestive HF
HTN
Age >75 (2), >65 (1)
Diabetes
Stroke/TIA/VTE
Vascular disease
Sex (Female)

Question 163

Where is access preferred for PCI?

Answer 163

Radial artery

Question 164

Which medications can worsen glucose tolerance?

Answer 164

Thiazides

Question 165

widespread pansystolic murmur, hypotension, pulmonary oedema post MI?

Answer 165

Acute mitral regurg

Question 166

Management of suspected HF in GP?

Answer 166

Measure BNP and refer for TTE if elevated

Question 167

What does a loud opening snap indicate?

Answer 167

The mitral valve leaflets are still mobile in mitral stenosis

Question 168

What can indicate the severity of the mitral stenosis?

Answer 168

Length of murmur increases

Question 169

What are components of orbit score?

Answer 169

• Haemoglobin
• Age
• Bleeding history
• Renal impairment
• Treatment with anti platelets

Question 170

Nailed pulsation?

Answer 170

Quincke’s sign -> aortic regurgitation

Question 171

Rate control for AF?

Answer 171

Beta blocker
CCB
Digoxin

Question 172

Management of continued pain post PCI for MI?

Answer 172

Urgent CABG

Question 173

Reverse nike sign?

Answer 173

Digoxin

Question 174

Persistent ST elevation post MI?

Answer 174

Left ventricular aneurysm

Question 175

What are signs of aortic coarctation?

Answer 175

• radio-femoral delay
• mid systolic murmur
• weak peripheral pulses in legs
• Left ventricular heave

Question 176

Investigations to confirm aortic coarctation?

Answer 176

• Echo
• CT aorta
• Cardiac catheterisation

Question 177

Management options for aortic coarctation?

Answer 177

• Open surgery
• Balloon angioplasty and stent insertion
• Mild cases can be controlled with antihypertensives

Question 178

What carries the worst prognosis in symptomatic aortic stenosis?

Answer 178

Exertional syncope

Question 179

What medication should be avoided in someone with aortic stenosis?

Answer 179

Nitrates

Question 180

When should adenosine be avoided?

Answer 180

Asthmatics

Question 181

What is the definitive management of bradycardia?

Answer 181

Permanent pacemaker

Question 182

Which organisms often cause rheumatic fever?

Answer 182

Strep pyogenes

Question 183

Stroke + AF?

Answer 183

2 weeks of aspirin then warfarin/DOAC

Question 184

ADPKD is associated with what?

Answer 184

Mitral valve prolapse

Question 185

S3 vs S4 sounds

Answer 185

CCF - 3 letters - S3
HOCM - 4 letters - S4

Question 186

What does aortic dissection cause?

Answer 186

Weak/absent carotid, brachial or femoral pulses

Question 187

HF with rEF vs HF with pEF?

Answer 187

rEF - systolic dysfunction e.g. IHD, arrythmias
pER - diastolc dysfunction e.g. HOCM, cardiac tamponade

Question 188

What can be done for patients not responding to medications for HF?

Answer 188

Cardiac resynchronisation therapy if wide QRS

Question 189

Raised JVP, ankle oedema, hepatomegaly

Answer 189

Right sided HF

Question 190

What are causes of torsades de pointes?

Answer 190

• Congenital
• Macrolides
• Subarachnoid haemorrhage
• Hypothermia
• Electrolyte disturbances

Question 191

What is torsades de pointes?

Answer 191

Polymorphic VT

Question 192

Heart failure management

Answer 192

1. ACE + BB
2. Spironolactone/Eplerenone

3rd lines
- Ivabradine if HR > 75 and reduced EF
- Hydralazine with nitrate for Afro-Caribbean patients
- Sacubitrtil-valsartan for patients with reduced EF after ACE/ARB wash out period
- Digoxin if sinus rhythm

Question 193

What vaccines should be given to HF patients?

Answer 193

Annual flu
One off PCV

Question 194

Sudden heart failure, raised JVP, pulsus parodoxus post MI?

Answer 194

Left ventricular free wall rupture

Question 195

What ABG picture will hyperaldosteronism cause?

Answer 195

Metabolic alkalosis with hypokalaemia

Question 196

What can cause high output heart failure?

Answer 196

Anaemia

Question 197

When is DC cardioversion done for arrhythmias?

Answer 197

Systolic < 90

Question 198

How to manage HTN when patient is on ACE/CCB/Thiazide and K+ > 4.5?

Answer 198

Add alpha/beta blocker

Question 199

AF with sudden onset abdo pain?

Answer 199

Think acute mesenteric ischaemia -> treat with immediate laparotomy

Question 200

Management of ruptured AAA?

Answer 200

Crossmatch 6 units of blood

Question 201

When is amiodarone preferred for pharmacological cardioversion?

Answer 201

Evidence of structural heart disease

Question 202

Chest pain + neurology?

Answer 202

Think aortic dissection

Question 203

new BP >= 180/120 mmHg + new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

Answer 203

Refer for assessment

Question 204

CCB side effects

Answer 204

headache, flushing, ankle oedema

Question 205

Amlodipine can cause what?

Answer 205

Gingival hyperplasia

Question 206

What is the cut off for aortic valve surgery if no symptoms?

Answer 206

Valvular gradient > 40 with features of left systolic dysfunction

Question 207

pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles

Answer 207

Wolf-Parkinson-White

Question 208

Gallop rhythm is a sign of what?

Answer 208

Left sided heart failure

Question 209

Prosthetic vs mechanical valve?

Answer 209

Mechanical last longer so are given to younger patients

Question 210

What can be considered in CPR if a PE is supected?

Answer 210

Thrombolytic drugs such as alteplase

Question 211

How should 80+ year olds with raised BP be managed?

Answer 211

Lifestyle advice

Question 212

Nifedipine can cause what?

Answer 212

Peripheral vasodilation which can cause reflex tachycardia

Question 213

What is an alternative to amiodarone in arrest?

Answer 213

Lidocaine

Question 214

What drugs are an alternative to atropine?

Answer 214

Isoprenaline/adrenaline infusion

Question 215

How long should CPR be continued when thrombolytic drugs are being given?

Answer 215

60-90 minutes

Question 216

Tension pneumothorax can cause what?

Answer 216

Pulseless electrical activity

Question 217

Clinically unstable aortic dissection?

Answer 217

Transoesophageal echo

Question 218

What is the most common cause of aortic stenosis in young patients?

Answer 218

Congenitally bicuspid valve

Question 219

Hyperlipidaemia can cause what?

Answer 219

Pseudohyponatremia -> serum osmolality will be normal

Question 220

Premature supraventircular beats vs premature ventricular betas on ECG?

Answer 220

Supraventricular - narrowed QRS complexes
Ventricular - widened QRS complexes

Question 221

What is cardiac tamponade?

Answer 221

Accumulation of pericardial fluid causing increased pericardial pressure which compromises ventricular filling, resulting in a
reduced cardiac output.

Question 222

cardiomyopathy + diabetes + joint pain + hepatomegaly

Answer 222

Think haemochromatosis

Question 223

What antibiotic is recommended in COPD patients who continue to have exacerbations?

Answer 223

Azithromycin

Question 224

Chronic infection with Pseudomonas and Bulkholderia in CF

Answer 224

Increased risk of morbidity or mortality

Question 225

Pericarditis vs STEMI ECG?

Answer 225

STEMI will have ST elevation greater in lead III than lead II

Question 226

Aortic dissection can cause what?

Answer 226

Neuro deficits

Question 227

Persistent ST elevation with fatigue

Answer 227

Left ventricular aneurysm

Question 228

When do CK levels normalise after an MI?

Answer 228

48-72 hours -> good to check if suspecting a reinfarction

Question 229

When should sacubitril-valsartan be initiated?

Answer 229

Following an ACE/ARB wash out period

Question 230

What part of the QRS is electrical cardioversion synchronised to?

Answer 230

R wave

Question 231

Mitral regurg is associated with which conditions?

Answer 231

• Marfans
• Ehlers-Danlos

Question 232

DC cardioversion vs unsynchronised cardioversion?

Answer 232

DC- Tachyarrhythmias
Unsynchronised - Cardiac arrest (VT, VF)

Question 233

What is the management of atrial flutter?

Answer 233

1. Beta blocker/CCB
2. Consider cardioversion
3. Catheter ablation curative

Question 234

Sudden increase in BP associated with ACS?

Answer 234

Treat with IV GTN

Question 235

Elderly patient with ECG with periods of sinus bradycardia + atrial tachycardia?

Answer 235

Sick sinus syndrome

Question 236

What is a normal PR interval?

Answer 236

0.12-0.20s
3-5 small squares

Question 237

Absent P waves + regular rhythm of QRS

Answer 237

SVT

Question 238

What stroke is most likely during cardiac catheterisation?

Answer 238

Embolic -> debris can be scraped from aortic wall

Question 239

Most common cause of left ventricular hypertrophy in a healthy person?

Answer 239

Hypertrophic cardiomyopathy

Question 240

Heart failure + wide QRS?

Answer 240

Consider resynchronisation pacemaker device

Question 241

2nd line investigation for endocarditis if echo is negative but high suspicion?

Answer 241

PET CT

Question 242

What is the PR interval?

Answer 242

Start of P wave to start of QRS complex

Question 243

Indications for DC cardioversion in tachyarrhythmias except shock?

Answer 243

• Syncope
• MI
• Heart failure

Question 244

What are the 2 options for aortic valve replacement?

Answer 244

Surgical - low risk patients
Transcatheter - high risk patients

Question 245

When to do 1 shock vs 3 shocks in shockable rhythms?

Answer 245

3 shocks - if witness cardiac arrest
1 shock - if not witnessed

Question 246

What is a common cause of tricuspid regurg?

Answer 246

Pulmonary HTN e.g. COPD

Question 247

Investigation of choice for cardiac tamponade?

Answer 247

Echo

Question 248

When in CABG indicated?

Answer 248

More significant coronary artery disease e.g. triple vessel

Question 249

Abx for MRSA resistant endocarditis?

Answer 249

Prosthetic valve - Vancomycin, Rifampicin and Gentamicin
Normal valve - Vancomycin and Rifampicin

Question 250

Thiazides can precipitate what?

Answer 250

Digoxin toxicity

Question 251

De Musset sign is a sign of what?

Answer 251

Aortic regurgitation

Question 252

What is acute coronary syndrome? (ACS)

Answer 252

umbrella term covering number of acute presentations of ischaemic heart disease

Question 253

Presentations of acute coronary syndrome?

Answer 253

1) STEMI
2) NSTEMI
3) unstable angina

Question 254

As a rise in troponins may take hrs, it may be hard to distinguish between unstable angina and NSTEMI initally so what do you do?

Answer 254

Treat like NSTEMI until troponin result is known

Question 255

When is unstable angina considered to be present in patients? (an acute coronary syndrome)

Answer 255

pts with ischaemic symptoms suggestive of ACS and NO elevation in troponins, with or without ECG changes indicative of ischaemia

Question 256

ACS generally develops in what patients?

Answer 256

Those with known or unknown ischaemic heart disease

Question 257

What are other terms for ischaemic heart disease (all have the SAME meaning)?

Answer 257

coronary heart disease, coronary artery disease, IHD all mean same thing

Question 258

What causes IHD?

Answer 258

gradual build up of fatty plaques within walls of coronary arteries

Question 259

What does IHD lead to?

Answer 259

1) gradual narrowing of coronary arteries therefore less oxygen reaching myocardium at times of increased demand -> angina

2) risk of sudden plaque rupture -> sudden occlusion of coronary artery -> no oxygen reaching area of myocardium

Question 260

Unmodifiable RFs for IHD

Answer 260

increasing age, male, FHx

Question 261

Modifiable RFs for IHD

Answer 261

smoking, DM, HTN, obesity, hypercholesterolaemia

Question 262

IDH pathophysiology: inital endothelial dysfunction is triggered by what?

Answer 262

factors eg. smoking, HTN, hyperglycaemia

Question 263

Inital endothelial dysfucntion results in what changes to the endothelium in IHD?

Answer 263

pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability

Question 264

IHD pathophysiology: endothelial dysfunction is triggered and there are a number of changes to the endothelium; fatty infiltration of the subendothelial space by what then occurs?

Answer 264

Low-density lipoprotein (LDL) particles

Question 265

IHD pathophysiology: role of monocytes in the progagation of the inflammatory process?

Answer 265

monocytes migrate from the blood and differentiate into macrophages; these then phagocytose oxidised LDL, slowly turning into large ‘foam cells’. As these macrophages die, the result can further propagate the inflamm process

Question 266

IHD pathophysiology: what forms the fibrous capsule covering the fatty plaque?

Answer 266

smooth muscle proliferation and migration from tunica media into intima results in formation of fibrous capsule covering fatty plaque

Question 267

What pathophysiological changes can be seen in IHD over number of years?

Answer 267

• intial endothelial dysfunction
• results in a number of changes to endothelium
• fatty infitration of subendothelial space by LDL
• formation of ‘foam cells’ and inflammatory process
• smooth muscle proliferation and migration to form fibrous capsule covering fatty plaque

Question 268

Cx of atherosclerosis?

Answer 268

angina
MI

Question 269

How does atherosclerosis cause angina?

Answer 269

plaque forms physical blockage in lumen of coronary artery; may cause reduced blood flow (and so oxygen) to myocardium, partically at times of increased demand

Question 270

How can atherosclerosis cause myocardial infarction?

Answer 270

plaque may rupture, potentially causing a complete occlusion of coronary artery

Question 271

Function of endothelium of arteries?

Answer 271

protects vessel wall and prevents clotting

Question 272

Pathophysiology of atherosclerosis?

Answer 272

• damage to endothelium wall allows LDL to enter
• monocytes enter and break LDL down by oxidation, causes macrophage to die
• then deposits under damaged endothelium: called foam cells
• when macrophages die, also release cytokines that causes more monocytes to enter endothelium and break down more LDL
• foam cells build up to form a lesion called a fatty streak
• fatty streak is thrombogenic meaning blood can clot on it
• platelets gather at damaged endothelium and release platelet dervived growth factor which encourages growth of smooth muscle cells
• smooth muscle meant to stay in middle layer (tunica media) but starts to growth in tunica intima where they multiply
• smooth muscle cells secrete collagen, proteoglycans, elastin fibrous cells that form a wall around fatty streak preventing blood clotting= extracellular matrix wall of fibrous cap
• fibrous cap + fatty streak = plaque

Question 273

Why in atherosclerosis do the walls of the arteries become stiff?

Answer 273

• smooth muscle also starts depositing calcium into the plaque creating crystals
• Ca crystals normally deposited by LDL and removed by HDL, but plaque stops HDL removing Ca
• causes build up of Ca in vessel wall and crystallises= stiffens walls of arteries

Question 274

Why might a high CRP indicate atherosclerosis?

Answer 274

atherosclerosis is an inflamm disease as immune sysytem invl (macrophages). Therefore high CRP

Question 275

CPS of acute coronary syndrome?

Answer 275

• left-sided/central chest pain
• may radiate to jaw or L arm
• ‘crushing’ ‘heavy’
• dyspnoea
• sweating
• nausea

Question 276

What pts with ACS may not experience any chest pain?

Answer 276

Diabetics; elderly

Question 277

Physical signs of ACS

Answer 277

• BP, HR, T, O2 often normal or mild eg. tachy
• unless HF
• pale, clammy

Question 278

Most important Ix when assessing pt with chest pain

Answer 278

• ECG
• cardiac markers eg. troponin

Question 279

Deep and widespread ST depression is associated with what?

Answer 279

very high mortality because it signifies severe ischaemia usually of LAD or left main stem

Question 280

Aims of treatment of ACS?

Answer 280

1) prevent worsening (further occlusion)
2) revascularise (unblock) vessel if occluded (STEMI)
3) Mx pain

Question 281

Acute Mx of ACS

Answer 281

M.orphine (IV)
O.xygen (if <94%)
N.itrates (IV or subling)
A.spirin (300mg)

Question 282

When should oxygen be given in Mx of ACS?

Answer 282

if sats <94%

Question 283

Secondary prevention for pts who have had an ACS?

Answer 283

Aspirin
Antiplatelet eg. clopidogrel
BB
ACE inhibitor
Statin

Question 284

STEMI?

Answer 284

ST-elevation MI= ST-segment elevation + elevated biomarkers of myocardial damage

Question 285

NSTEMI?

Answer 285

non ST-elevation MI= ECG change but no ST-segment elevation + elevated biomarkers of myocardial damage

Question 286

Groups of Mx for acute coronary syndromes?

Answer 286

• STEMI
• NSTEMI/unstable angina
• Secondary prevention

Question 287

Dose of aspirin to give in acute Mx?

Answer 287

300mg

Question 288

Acute Mx of ACS: nitrates should be used in caution if the pt is…

Answer 288

Hypotensive

Question 289

Overview of Mx in pt with suspected ACS?

Answer 289

1) acute Mx
2) ECG findings- ?STEMI
3) STEMI confirmed= eligability for coronary reperfusion therapy

Question 290

STEMI criteria?

Answer 290

CP consistent with ACS ≥ 20mins with persistent >20mins ECG features in ≥ 2 contiguous leads

Question 291

STEMI ECG criteria in men?

Answer 291

ECG features in ≥ 2 contiguous leads of….

Men <40yrs=
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3

Men >40yrs= ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3

PLUS 1 mm ST elevation in other leads & new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 292

STEMI ECG criteria in women?

Answer 292

ECG features in ≥ 2 contiguous leads of…

1.5 mm ST elevation in V2-3

Question 294

STEMI Mx?

Answer 294

1) 300mg aspirin (+other acute Mx)

2) PCI OR Fibrinolysis

3) dual antiplatelet therapy: Clopidogrel + aspirin (if high bleeding risk) or tricagrelor + aspirin (low risk)

4) stenting indicated? Cardiac rehab and secondary prevention

Question 295

2 types of coronary reperfusion therapy in STEMI?

Answer 295

1) PCI: dual antiplatelet therapy before; then during give either unfractionated heparin with bailout GPI if radial access or bivalirudin with bailout GPI if femoral access

2) Fibrinolysis + antithrombin drug

Question 296

In STEMI Mx when should pt get PCI?

Answer 296

<12hrs of symptoms and can be delivered in 120mins. Consider >12hrs if CG shock or continue ischaemia.

Question 297

PCI for Mx of STEMI?

Answer 297

1) dual antiplatelet therapy before PCI:
aspirin + prasugrel or clopidogrel

2) PCI with radial access: + unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)

OR

2) PCI with femoral access: bivalirudin with bailout GPI

Question 298

Dual antiplatelet therapy to give pt with STEMI prior to PCI?

Answer 298

Aspirin +
clopidogrel if taking oral anticoag
or
prasugrel if not taking oral anticoag

Question 299

In STEMI Mx when should pt get fibrinolysis?

Answer 299

if <12hrs and PCI not possible in 120mins

Question 300

Patients undergoing fibrinolysis should also be given what?

Answer 300

Antithrombin drug eg. fondaparinux or LMWH

Question 301

When should ECG be done after fibrinolysis?

Answer 301

60-90mins after

Question 302

STEMI Mx: is radial or femoral access preferred?

Answer 302

Radial

Question 303

What if pt with STEMI gets ECG 90mins after fibrinolysis and it fails to show resolution of ST elevation?

Answer 303

PCI

Question 304

Mx of NSTEMI/unstable angina overview?

Answer 304

1) 300mg aspirin + fondaparinux or unfractionated heparin

2) GRACE score

3) low risk= dual antiplatelt therapy (aspirin + ticagrelor or clopidogrel)

3) intermediate/high risk= PCI immediately/within 72hrs; give aspirin + prasugrel or ticagrelor (if pt on oral anticoag give clopidogrel); give unfractioned heparin; use drug-eluting stents

4) assess LV function and consider angiography (eg. if develop ischaemia)

5) cardiac rehab and secondary prevention

Question 305

What is dual antiplatelet therapy (DAPT)?

Answer 305

aspirin + P2Y12 inhibitor eg. clopidogrel, prasugrel or ticagrelor

Question 306

How to know what drugs to use for DAPT?

Answer 306

Apirin +

prasugrel (during PCI) if not taking anticoag

clopidgorel (during PCI) if taking anticoag

ticagrelor if low bleeding risk

clopidogrel if high bleeding risk

Question 307

How do you decide if you use fonaparinux or unfractionated heparin initally in the Mx of NSTEMI/unstable angina?

Answer 307

• fondaparinux= low risk of bleeding and no immediate angiography
• unfractionated heparin= immediate angiography planned or creatinine is > 265 µmol/L

Question 308

What does GRACE score stand for?

Answer 308

The Global Registry of Acute Coronary Events

Question 309

What is the GRACE score?

Answer 309

Predicts 6m mortality and risk of cardiovascular events

Question 310

In Mx for NSTEMI/unstable angina, as well as the GRACE risk score what else needs to be included in the risk assessment?

Answer 310

history, examination; ECG; bloods (troponin I or T, creatinine, glucose, Hb); balance possible benefits of Mx against bleeding risk

Question 311

What factors does the GRACE score account for?

Answer 311

age
HR, BP
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

Question 312

GRACE score: what is low risk?

Answer 312

predicted 6m mortality ≤ 3%

Question 313

GRACE score: what is intermediate or higher risk?

Answer 313

predicted 6-month mortality > 3%

Question 314

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) immediateley?

Answer 314

clinically unstable eg. hypotensive

Question 315

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) within 72hrs?

Answer 315

pts with GRACE score >3%

Question 316

When should coronary angiography be considered for pts with NSTEMI/unstable angina?

Answer 316

if ischaemia is experienced after admission

Question 317

What is cardiac rehabilitation used as the final Mx for ACS?

Answer 317

before discharge; assessment 10days after discharge

physical activity, lifestyle advice, stress management and health education

Question 318

Drug therapy for secondary prevention for ACS (STEMI, NSTEMI, unstable angina)?

Answer 318

• ACE inhibitor
• DAPT
• Beta-blocker
• Statin

Question 319

DAPT for secondary prevention of ACS?

Answer 319

Aspirin + second antiplatelet for up to 12m

Question 320

Drug titration of beta-blockers for secondary prevention of ACS?

Answer 320

titrate to max tolerated or target dose

Question 321

Drug titration for ACE inhibitors for secondary prevention of ACS?

Answer 321

titrate up (with monitoring) every 12-24hrs; complete titration in 4-6w of hospital discharge.

Question 322

What should you monitor in pts before starting and 1-2w after starting an ACE inhibitor?

Answer 322

renal function, electrolytes and BP

Question 323

Secondary prevention for ACS: if pt already on anticoag, offer clopidogrel for how long?

Answer 323

Up to 12m if had PCI

Question 324

Poor prognostic factors of ACS?

Answer 324

age; Hx or development of HF; PVD; reduced systolic blood pressure; Killip class; inital serum creatinine conc; elevated initial cardiac markers; cardiac arrest on admission; ST segment deviation

Question 325

What is the name of the system used to stratify risk post MI?

Answer 325

Killip class

Question 326

Killip class features and 30 day mortality?

Answer 326

I= no signs HF (6%)
II= lung crackes, S3 (17%)
III= frank pulmonary oedema (38%)
IV= cardiogenic shock (81%)

Question 327

Cx of myocardial infarction?

Answer 327

Cardiac arrest
Cardiogenic shock
Chronic heart failure
Tachyarrhythmias
Bradyarrhythmias
Pericarditis
Left ventricular aneurysm
LV free wall rupture
Ventricular septal defect
Acute mitral regurgitation

Question 328

Most common cause of death following MI

Answer 328

Cardiac arrest

Question 329

Why can cardiac arrest occur after MI?

Answer 329

pt develops ventricular fibrillation

Question 330

Cardiac arrest Mx

Answer 330

ALS with defibrillation

Question 331

Why may pt develop cardiogenic shock after MI?

Answer 331

if large part of V myocardium damaged by infarction the EF may decrease to the point the pt develops CG shock

Question 332

Causes of cardiogenic shock?

Answer 332

post MI; mechanical Cx (LV free wall rupture)

Question 333

Pt with cardiogenic shock may require what?

Answer 333

Inotropic support and/or intra-aortic balloon pump

Question 334

Cardiogenic shock?

Answer 334

Heart suddenly can’t pump enough blood to meet body’s needs as it has been damaged so much. Life-threatening- can lead to organ failure.

Question 335

Why may MI lead to chronic HF?

Answer 335

ventricular myocardium may be damaged and dysfunctional

Question 336

Arrhythmias that may develop post MI?

Answer 336

Ventricular fibrillation (most common cause of death following MI); ventricular tachy; bradyarrhythmias

Question 337

Atrioventricular block is more common following what type of MI?

Answer 337

Inferior

Question 338

What is common (10%) in first 48hrs following a transmural MI?

Answer 338

Pericarditis

Question 339

Pain worse lying flat and better leaning forward; pericardial rub may be heard; may see pericardial effusion on echo

Answer 339

Pericarditis

Question 340

Dressler’s syndrome?

Answer 340

Pericarditis that can occur 2-6w following an MI.

Question 341

Fever, pleuritic pain, pericardial effusion and raised ESR?

Answer 341

Dressler’s

Question 342

Pathophysiology of Dressler’s?

Answer 342

autoimmune reaction against antigenic proteins formed as myocardium recovers

Question 343

Mx of dressler’s?

Answer 343

NSAIDs

Question 344

Ischaemic damage following MI may weaken the myocardium and result in LV aneurysm forming. What is this associated with?

Answer 344

Persistent ST elevation and LV failure.

Question 345

Why may LV aneurysm increase risk of stroke?

Answer 345

thrombus may form within the aneurysm

Question 346

Pts with LV aneurysm are what?

Answer 346

Anticoagulated

Question 347

When could a LV free wall rupture occur after MI?

Answer 347

1-2w after (3% of MIs)

Question 348

Acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)?

Answer 348

LV free wall rupture

Question 349

Mx for LV free wall rupture?

Answer 349

urgent pericardiocentesis and thoracotomy

Question 350

Pulsus paradoxus?

Answer 350

When BP decreases with inhalation eg. in cardiac tamponade

Question 351

When would rupture of interventricular septum occur post MI (1-2% pts)?

Answer 351

in 1st week

Question 352

Features of ventricular septal defect post MI?

Answer 352

Acute HF associated with pan-systolic murmur

Question 353

Diagnosis of ventricular septal defect post MI?

Answer 353

ECHO diagnostic and will exclude acute mitral regurg (presents similar)

Question 354

Mx of ventricular septal defect post MI?

Answer 354

Urgent surgical correction

Question 355

What may cause acute mitral regurgitation post MI?

Answer 355

infero-posterior infarction and may be due to ischaemia or rupture of papillary muscle

Question 356

CP of mitral regurg post MI?

Answer 356

acute hypotension, pulmonary oedema; early-mid systolic murmur

Question 357

Mx for pt with mitral regurg post MI?

Answer 357

vasodilator therapy but often require emergency surgical repair.

Question 358

Secondary prevention of ACS: dietary advice?

Answer 358

Mediterranean style diet; switch butter and cheese for plant oil based products; do NOT recommend eating oily fish

Question 359

Secondary prevention of ACS: exercise advice?

Answer 359

20-30mins a day until pt slightly breathless

Question 360

When can sexual activity resume after an uncomplicated MI?

Answer 360

4w after. Sex does not increase likelihood of further MI

Question 361

When can PDE5 inhibitors eg. sildenafil be used in pts post MI?

Answer 361

6m after MI but avoid in pts prescribed nitrates or nicorandil

Question 362

DAPT post ACS?

Answer 362

aspirin + ticagrelor (stop T after 12m)

Question 363

DAPT post PCI?

Answer 363

aspirin + prasugrel or ticagrelor (stop P or T after 12m)

Question 364

When might the 12m period for DAPT be altered in patients?

Answer 364

If at high risk of bleeding or high risk of further ischaemic events

Question 365

What should be initiated after ACE inhibitor theraoy in pts who had an acute MI and have symptoms/signs of HF and LV systolic dysfunction for secondary prevention?

Answer 365

Aldosterone antagonists eg. eplerenone 3-14days post-MI

Question 366

Abdominal aortic aneurysm (AAA)?

Answer 366

Permanent pathological dilation of abdominal aorta with diameter >1.5 times the expected anteroposterior diameter of the segment given the person’s sex and body size

Question 367

Threshold for diagnosis of AAA?

Answer 367

abdo aortic diameter of 3cm or more

Question 368

RFs for AAA?

Answer 368

male, age, smoking, HTN, FHx, DM, COPD, hyperlipidaemia

Question 369

When is screening for AAA offered?

Answer 369

All men the yr they become 65yrs

Question 370

AAA screening test?

Answer 370

abdo USS to detect any bulging or swelling of aorta

Question 371

AAA screening: no aneurysm found?

Answer 371

<3cm- no further scans requried

Question 372

AAA screening: small AAA?

Answer 372

3-4.4cm. Placed under surveillance and repeat scan in 12m (repeat every 12m)

Question 373

AAA screening: medium AAA?

Answer 373

4.5-5.4cm. Under surveillance and repeat scan in 3m (repeat every 3m)

Question 374

AAA screening: large AAA?

Answer 374

5.5cm+. Referred to vascular surgeon within 2w for probable intervention.

Question 375

How long does AAA screening take?

Answer 375

15mins; told results at appointment

Question 376

Why is there screening for AAA?

Answer 376

majority asymptomatic and if rupture then high mortality.

Question 377

What AAA have a low rupture risk?

Answer 377

asymptomatic, diameter <5.5cm (small and medium)

Question 378

High rupture risk AAA?

Answer 378

Symptomatic, diameter >=5.5cm or rapidly enlarging (>1cm/yr)

Question 379

How are large high risk AAA surgically managed?

Answer 379

Elective endovascular repair (EVAR) or open repair. EVAR stent placed into abdo aorta via femoral artery to prevent blood from collecting in aneurysm

Question 380

Cx of EVAR for AAA?

Answer 380

endo-leak: stent fails to exclude blood from aneurysm; asymptomatic on routine follow up

Question 381

Why do AAA occur?

Answer 381

As result of the failure of elastic proteins in the matrix.

Loss of intima with loss of elastic fibres from the media, associated with increased proteolytic activity and lymphocytic infiltration.

Question 382

Normal diameter abdo aorta in men and women >50yrs?

Answer 382

F: 1.5cm
M: 1.7cm

Question 383

Aneurysms typically represent dilation of…

Answer 383

all layers of the arterial wall; most caused by degenerative disease

Question 384

Rare causes of AAA?

Answer 384

Syphilis; connective tissue disorders eg. Ehlers Danlos type 1 and Marfan’s

Question 385

Peripheral arterial disease (PAD)?

Answer 385

narrowing or occlusion of peripheral arteries affecting blood supply to lower limbs

Question 386

Types (symptoms) of peripheral arterial disease?

Answer 386

Acute limb ischaemia
Intermittent claudication
Chronic limb-threatening ischaemia
Asymptomatic

Question 387

PAD: acute limb ischaemia?

Answer 387

sudden decrease in limb perfusion that threatens limb viability- CP <2w

Question 388

PAD: intermittent claudication?

Answer 388

diminished circulation leads to pain in lower limb on walking or exercise, relieved on rest

Question 389

Most common symptom of PAD?

Answer 389

Intermittent claudication

Question 390

PAD: chronic limb-threatening ischaemia?

Answer 390

chronic, inadequate tissue perfusion at rest and is defined by ischaemic rest pain, with or without tissue loss

Question 391

Asymptomatic PAD?

Answer 391

early stage in the condition and may progress with symptoms of intermittent claudication or chronic limb-threatening ischaemia

Question 392

PAD of the lower limbs is most commonly caused by?

Answer 392

Atherosclerosis

Question 393

Cause of acute limb ischaemia (PAD)?

Answer 393

thrombosis within diseased artery when plaque ruptures

Question 394

RFs for PAD?

Answer 394

smoking, DM, HTN, hypercholesterolaemia

Question 395

CP of acute limb ischaemia (PAD)?

Answer 395

pain, pallor, pulseless, perishing with cold, paraesthesia and power loss

Question 396

CP of chronic limb ischaemia (PAD)?

Answer 396

progressive development of cramp-like pain in calf, thigh or buttock on walking; not relieved by rest; unexplained foot or leg pain; non-healing wounds on lower limb. ?absent foot pulses.

Question 397

Pt with pain in leg worse at night, sleep with leg hanging out of bed or sleep in a chair?

Answer 397

Chronic limb-threatening ischaemia

Question 398

Why do pts with chronic limb-threatening ischaemia report pain worse at night?

Answer 398

decrease of BP when asleep and no gravity when lying down

Question 399

CP of intermittent claudication (PAD)?

Answer 399

pain in lower limb on walking or exercise, relieved by rest (within 10mins), aching, burning, distal extremity before proximal. Uni or bilateral

Question 400

Ix for PAD?

Answer 400

ankle brachial pressure index (ABPI)

Question 401

What reading of an ABPI suggests the presence of PAD?

Answer 401

0.9 or less

Question 402

Mx of acute limb ischaemia?

Answer 402

ABC, IV opioids, IV unfractionated heparin then:

Urgent assessment by vascular specialist: endovascular therapies (eg. percutaneous catheter-directed thrombolytic therapy) or surgical interventions (eg. surgical thromboembolectomy)

Question 403

Mx of chronic limb-threatening ischaemia?

Answer 403

• urgent referral to vascular
• pain Mx: paracetamol, weak/strong opioids
• advice

Question 404

Mx of intermittent claudication?

Answer 404

• supervised exercise programme (2hrs per w for 3m)
• lifestyle advice
• referral for consideration of angioplasty or bypass surgery
• if don’t want surgery= naftidrofurl oxalate

Question 405

What if supervised exercise programme is not available in pts with intermittent claudication?

Answer 405

30mins exercise 3-5 times per week; walking until onset of symptoms then rest

Question 406

All people with PAD should be given what?

Answer 406

Advice and treatment for secondary prevention of CVD

Question 407

Physical signs in someone with PAD?

Answer 407

dry shiny skin; elevation pallor; hair loss over dorsum of foot; muscle atrophy; thickened toenails; ulceration on heel

Question 408

Ruptured AAA?

Answer 408

catastrophic (sudden collapse) or sub-acute (persistent severe central abdo pain with developing shock). 80% mortality

Question 409

CP of ruptured AAA?

Answer 409

severe central abdo pain radiating to back; pulsatile expansile mass in abdo; may be shocked (hypoten, tachy) or collapsed

Question 410

Severe central abdo pain radiating to back?

Answer 410

ruptured AAA

Question 411

Ruptured AAA Mx?

Answer 411

immediate vascular review for emergency surgical repair.

if stable may get CT angiogram to confirm

Question 412

Tear in the tunica intima of the wall of the aorta

Answer 412

aortic dissection

Question 413

Associations with aortic dissection?

Answer 413

HTN
trama; bicuspif aortic valve; marfans; turner’s and noonan’s; pregnancy; syphillis

Question 414

Severe and sharp tearing cheat and upper back pain

Answer 414

aortic dissection

Question 415

Aortic dissection CP

Answer 415

tearing sharp chest and upper back pain; weak or absent pulse; variation (>20) in SBP between arms; aortic regurg; HTN

Question 416

Aortic dissection if involves cornonary/spinal arteries/distal aorta?

Answer 416

1) anginga
2) paraplegia
3) limb ischaemia

Question 417

Are there ECG changes in aortic dissection?

Answer 417

non-specific or no ECG changes. Some: ST-elevation in inferior leads

Question 418

Stanford classification of aortic dissection?

Answer 418

• Type A (2/3)= ascending aorta
• Type B (1/3)= descending aorta, distal to L subclavian origin

Question 419

Ix for aortic dissection?

Answer 419

• CT angiography of chest, abdo and pelvis GOLD (if stable)
• Tranoesophageal echo (if unstable)
• CXR: widened mediastinum

Question 420

Finding on CT angiography of chest, abdo and pelvis for aortic dissection?

Answer 420

False lumen

Question 421

Mx for Type A aortic dissection?

Answer 421

• surgery but BP must be controlled of S target of 100-120 whilst awaiting

Question 422

Mx for Type B aortic dissection?

Answer 422

conservative, bed res, reduce BP IV labetalol to prevent progression

Question 423

Complications of a backward tear in aortic dissection?

Answer 423

aortic incompetence/regurg
MI: inferior due to right cornonary invol.

Question 424

Complications of a forward tear in aortic dissection?

Answer 424

unequal arm pulses and BP; stroke; renal failure

Question 425

Aortic regrurg is the leaking of the aortic valve of heart that causes….

Answer 425

blood to flow in reverse direction during ventricular diastole

Question 426

What can cause aortic regurg?

Answer 426

disease of aortic valve or dilation of aortic root and ascending aorta

Question 427

Causes of aortic regurg due to valve disease?

Answer 427

Chronic= RF, calcific valve disease, connective tissue diseases (RA, SLE), bicuspid aortic valve

Acute= infective endocarditis

Question 428

Causes of aortic regurg due to aortic root disease?

Answer 428

Chronic= bicuspid aortic valve, spondylarthropathies, HTN, syphilis, Marfan’s

Acute= aortic dissection

Question 429

What type of murmur is aortic regurgitation?

Answer 429

Early diastolic murmur

Question 430

Where is aortic regurg best heard?

Answer 430

loudest at the left sternal edge

Question 431

Features of aortic regurg?

Answer 431

• collapsing pulse
• wide pulse pressure
• early diastolic murmur

Question 432

Signs in aortic regurg?

Answer 432

Quincke’s sign (nailbed pulsation) and De Musset’s sign (head bobbing)

Question 433

What can you get in severe aortic regurg?

Answer 433

mid-diastolic Austin-Flint murmur: due to partial closure of anterior mitral valve cusps caused by regurg streams

Question 434

Ix for aortic regurg?

Answer 434

echo

Question 435

Mx for aortic regurg?

Answer 435

• medical Mx for any HF
• surgery if indicated

Question 436

Indications for surgery in aortic regurg?

Answer 436

symptomatic patients with severe AR
or
asymptomatic patients with severe AR who have LV systolic dysfunction

Question 437

What type of murmur is aortic stenosis?

Answer 437

Ejection systolic murmur; has crescendo-decrescendo quality.

Question 438

Where is aortic stenosis heard loudest?

Answer 438

over aortic valve (2nd R ICP) and commonly radiates to carotid arteries. Loudest on espiration and when pt is sitting forward

Question 439

CP of aortic stenosis

Answer 439

• slow rising pulse with narrow pulse pressure
• non-displaced heaving apex beat (LV hypertrophy)
• reduced or absent S2
• reverse splitting of S2

Question 440

Causes of aortic stenosis?

Answer 440

• degenerative calcification (>65yrs)
• bicuspid valve disease (<65yrs)
• RF
• William’s syndrome (supravalvular aortic stenosis)

Question 441

Crescendo vs decrescendo vs crescendo-decrescendo murmur?

Answer 441

C= murmur increases in intensity
D= decrease in intensity
C-D= increase in intensity followed by decrease in intensity

Question 442

Is aortic stenosis C, D or C-D?

Answer 442

Crescendo-decresendo

Question 443

Is aortic regurg C, D or C-D?

Answer 443

Decrescendo

Question 444

Is mitral regurg C, D or C-D?

Answer 444

Crescendo-decrescendo

Question 445

Is mitral regurg C, D or C-D?

Answer 445

Decrescendo

Question 446

Mx for aortic stenosis

Answer 446

• asymptomatic= observe
• symptomatic= valave replacement
• asymptomatic but valvular gradient >40mmHg and features eg. LV systolic dysfunction= valve replacement

Question 447

Mitral regurg occurs when blood leaks…

Answer 447

back through mitral valve on systole

Question 448

Where is mitral valve located?

Answer 448

between LA and V so regurg leads to less efficient heart as less blood pumped through body with each contraction

Question 449

What can happen as the degree of mitral regurg becomes more severe?

Answer 449

oxygen demand > heart can supply; leads to thicker myocardium; then fatigued when comes less efficient -> irreversible HF

Question 450

RFs for mitral regurg?

Answer 450

female, lower BMI, age, renal dysfunction, prior MI, prior mitral stenosis, collagen disorders

Question 451

Causes of mitral regurg?

Answer 451

post MI, mitral valve prolapse, infective endocarditis, RF, congenital

Question 452

What type of murmur is mitral regurg?

Answer 452

Pansystolic murmur heard loudest over apex and radiating to axilla. Severe may cause widely split S2.

Question 453

Where to listen for mitral regurg?

Answer 453

L 5th ICP mid-clav line; then left axilla.

Question 454

CP of mitral regurg?

Answer 454

most asymptomatic; symptoms due to failure of LV, arrythmias or pulmonary HTN so SOB, fatigue, oedema

Question 455

Ix for mitral regurg?

Answer 455

ECHO

• ECG: broad p
• CXR: cardiomegaly (enlarged LV and LA)

Question 456

What does mitral regurg sound like?

Answer 456

Like a high-pitched blowing, constant whoosh

Question 457

What can sometimes be felt with aortic stenosis?

Answer 457

palpable thrill

Question 458

What does aortic stenosis sound like?

Answer 458

Whoosh (starts soft, then loud, then soft again)

Question 459

Mx for mitral regurg?

Answer 459

Acute: nitrates, diuretics, +ve iontropes and intra-aortic balloon pump to increase cardiac output

Acute severe: surgical repair/replacement

Question 460

Mitral stenosis is when there is an obstruction of blood flow across…

Answer 460

the mitral valve from LA to LV; leads to high P in LA, pulmonary vessles and R heart

Question 461

Causes of mitral stenosis?

Answer 461

RHEUMATIC FEVER

Question 462

What type of murmur is mitral stenosis?

Answer 462

mid-late diastolic murmur best heard in expiration and loud in S1

Question 463

CP of mitral stenosis?

Answer 463

dyspnoea; haemoptysis (pink frothy or sudden haemorrhage); opening snap; low volume pulse; malar flush; AF

Question 464

What does an opening snap indicate in mitral stenosis?

Answer 464

mitral valve leaflets are still mobile

Question 465

Ix for mitral stenosis?

Answer 465

• echo: cross section of mitral valve <1sqcm (normal 4-6)
• cxr: may see LA enlargement

Question 466

Mx for mitral stenosis?

Answer 466

• asymptomatic= monitor regular with echo
• symptomatic= percutaneous mitral balloon valvotomy or mitral valve surgery
• if AF: warfarin

Question 467

Bicuspid aortic valve?

Answer 467

1-2% of population; asymptomatic in childhood

Question 468

The majority of pts with bicuspid aortic valve eventually develop what?

Answer 468

aortic stenosis or regurg; higher risk of aortic dissection and aneurysm formation (on ascending aorta)

Question 469

What is bicuspid aortic valve associated with?

Answer 469

a left dominant coronary circulation (posterior descending artery arises from circumflex not right coronary) and Turner’s

Question 470

Around 5% of patients with what also have coarctation of the aorta?

Answer 470

bicuspid aortic valve

Question 471

What are biological heart valves usually made from?

Answer 471

Bovine or porcine

Question 472

Disadvantage of biological heart valves?

Answer 472

structural deterioration and calcification over time; so >65/70yrs receive

Question 473

Is long-term anticoag needed for biological heart valves?

Answer 473

No; may give warfarin for first 3m; low-dose aspirin long term

Question 474

Most common type of mechanical heart valve?

Answer 474

Bileaflet valve

Question 475

Pro and con of mechanical heart valve?

Answer 475

low failure rate but increased risk of thrombosis so long term anticoag needed

Question 476

Is long term anticoag needed for mechanical heart valve?

Answer 476

Yes, warfarin

Question 477

Target INR for mechanical heart valve anticoag?

Answer 477

Aortic: 3.0
Mitral: 3.5

Question 478

Why do you manage pts with AF?

Answer 478

reduce the increased risk of stroke

Question 479

What is atrial fibrillation (a supraventricular tachyarrhythmia)?

Answer 479

uncoordinated atrial electrical activation and so ineffective atrial contraction, causing an irregular and abnormally rapid vetricular rhythm

Question 480

How would you describe the rhythm of AF?

Answer 480

Irregularly irregular

Question 481

Example of regularly irregular rhythm?

Answer 481

Ventricular ectopics

Question 482

Classification of AF?

Answer 482

• paraoxysmal (episodes terminate <7days of onset)
• persistent (>7d)
• longstanding persistent (>12m)
• permanent (no more attempts to restore sinus rhythm)

Question 483

RFs for AF and its maintenance?

Answer 483

HTN, IHD, HF, valvular disease, intercurrent illness, electrolyte disturbances, thyrotoxicosis, alcohol XS

Question 484

CP of AF

Answer 484

usually asymptomatic, undetected and undiagnosed

Question 485

Cx of AF?

Answer 485

stroke, HF, mortality, tachycardia-induced cardiomyopathy

Question 486

When should you suspect a diagnosis of AF?

Answer 486

irregular pulse with or without symptoms eg. SOB, palpitation, chest pain, dizziness, syncope

Question 487

Ix for AF?

Answer 487

• exam: pulse, auscultate heart and lungs
• ECG
• consider bloods, cxr, echo, ambulatory ecg monitoring (if paroxysmal AF)

Question 488

Routine review of someone with AF?

Answer 488

managing Cx; lifestyle modification; stroke and bleeding risk; monitor meds. Review symptoms, HR & rhythm, BP, adherence and adverse effects

Question 489

When should you arrange a prompt cardio referral in someone with AF?

Answer 489

recurrent or persistent symptoms despite rate and/or rhythm control treatment

Question 490

When to urgently admit someone to hospital with AF?

Answer 490

severe CP, haemodynamically unstable, decompensated HF

Question 491

When should you seek urgent cardio advice in someone with AF?

Answer 491

new onset within 48hrs, associated with structural disease or uncertainty about Mx

Question 492

Mx for pt with AF?

Answer 492

• assess stroke and bleeding risk
• lifestyle advice
• consider DOAC for stroke prevention eg. apixaban (or wafarin 2nd line)
• consider meds for rate control (BB or CCB)

Question 493

Signs of haemodynamic instability?

Answer 493

tachycardia (>150bpm); hypotension (S<90); severe dizziness, syncope, loss of consciousness; ischaemic chest pain or acute pulmonary oedema

Question 494

ECG for AF

Answer 494

absence of p waves, iregguarly-irregular R-R intervals,narrow QRS, ventricular rate 90-170bpm

Question 495

When should you arrange a transthoracic echo in someone with AF?

Answer 495

• high risk/suspicion of underlying functional or structural heart disease and this will influence Mx
• cardioversion (electrical or drug) is being considered

Question 496

Risk score for stroke?

Answer 496

CHA2DS2-VASc

Question 497

Assess pts bleeding risk?

Answer 497

ORBIT bleeding risk score

Question 498

When to offer a DOAC for pt with AF?

Answer 498

• chadvasc score 2 or more
• or if man and score of 1

Question 499

DOAC stands for and example?

Answer 499

direct-acting oral anticoag
apixaban, rivaroxaban

Question 500

What is warfarin?

Answer 500

vit KK antagonist; anticoag

Question 501

When to not offer rate control drug for pt with AF?

Answer 501

reversible cause; HF caused by AF; newonset AF <48hrs

Question 502

How to monitor pt on vit K antagonists eg. warfarin?

Answer 502

International normalised ratio (INR) until in therapeutic range

Question 503

What indicates that a pt on warfarin has sub-optimal anticoag control?

Answer 503

• TTR <65%
• 2 INR higher than 5, or one higher than 8 within 6m
• 2 IRN <1.5 within 6m

Question 504

What factors may cause sub-optimal anticoag control for pt on warfarin?

Answer 504

impaired cognitive function, poor adherence, acute illness, lifestyle eg. XS alcohol; medications

Question 505

What meds may interact with warfarn?

Answer 505

antiplatelets, SSRIs, NSAIDs

Question 506

When should you review someone who has just started rate control drugs eg. BB?

Answer 506

within 1 week of starting or each dose titration

Question 507

Ventricular rate targets for someone on rate control drugs eg. BB?

Answer 507

<80bom at rest and <110bpm during moderate exercise.
<100bpm at rest may be appropriate

Question 508

When is the highest risk for embolism leading to stroke in AF?

Answer 508

During cardioversion- thrombus in fibrillating atrium suddenly pushed out when sinus rhythm restored. SO make sure pt anticoag before (at least 3w prior)

Question 509

What is electrical cardioversion synchronised to?

Answer 509

R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when V fib can be induced

Question 510

Types of cardioversioN?

Answer 510

Electrical (DC cardioversion) or pharmacological eg. amiodarone, flecainide

Question 511

Following a TIA, when should anticoag for AF be started?

Answer 511

immediately once excluded haemorrhage

Question 512

In acute stroke pts, in absence of haemorrhage, when should anticoag for AF be started?

Answer 512

after 2w. In the intervening period give antiplatelet

Question 513

When should pt be electrically cardioverted if have AF?

Answer 513

if haemodynamically unstable

Question 514

Form of supraventricular tachy characterised by succession of rapid atrial depolarisation waves?

Answer 514

Atrial flutter

Question 515

Flutter waves in atrial flutter may be more visible following what?

Answer 515

carotid sinus massage or adenosine

Question 516

What features suggest VT rather than SVT?

Answer 516

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

Question 517

What does the Mx of bradycardia depend on?

Answer 517

1) presence of signs indicating haemodynamic compromise
2) potenial risk of asystole

Question 518

what factors indicate haemodynamic compromise and so the need for Mx in bradycardia?

Answer 518

• shock
• syncope
• MI
• HF

Question 519

Signs of shock?

Answer 519

hypotension (SBP <90), pallor, sweating, cold, clammy extremities, confusion, impaired consciousness

Question 520

Mx of bradycardia and tachycardia

Answer 520

• asssess with A-E
• give O2 if appropriate and gain IV access
• monitor ECG, BP, Sp02
• Treat any reversible causes eg. electrolyte abnorm
• any life threatening signs? (follow the different pathways)

Question 521

Life-threatening signs in someone with brady/tachy?

Answer 521

haemodynamically unstable; shock; syncope; MI; HF

Question 522

What may be signs that indicate risk of asystole (flat-line)?

Answer 522

• recent asystole
• Mobitz II AV block
• complete heart block with broad QRD
• V pause >3secs

Question 523

Mx for bradycardia with life threatening features?

Answer 523

Atropine 500mcg IV

Question 524

Mx if haemodynamically unstable with bradycardia and no response to atropine 500mcg IV or if there is a risk of asystole?

Answer 524

• repeat atropine up to 3mg
• isoprenaline 5mcg min-1 IV
• adrenaline 2-10mcg min-1 IV
• OR transcutaneuous pacing

Question 525

Mx for tachycardia if there are life threatening features?

Answer 525

Synchronised DC shock up to 3 attempts
- if unsuccessful: amiodarone 300mg IV over 10-30mins and repeat shock

Question 526

Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is irregular?

Answer 526

could be:
1) AF with BBB: same Mx as irregular narrow QRS tachy

2) polymorphic VT (eg. torsades)= gve Mg 2g over 10mins

Question 527

Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is regular?

Answer 527

1) VT (or uncertain)= amiodarone 300mg IV for 10-60min

2) previous diagnosis of SVT with BBB= Mx same as regular narrow QRS tachy

Question 528

Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is irregular?

Answer 528

1) ?AF= BB, anticaog if >48hrs and amiodarone if evidence of HF

Question 529

Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is regular?

Answer 529

1) vagal manoeuvre/fluids (normally decrease HR if sinus tachy)

if uneffective (usually SVT)

2) amiodarone 6mg rapid IV bolus, if unsuccessful give 12mg then if successful give 18mg AND monitor ECG
if uneffective
3) verapamil or BB

Question 530

What does supraventricular tachycardia (SVT) refer to?

Answer 530

any tachycardia that is not ventricular in origin

Question 531

SVT?

Answer 531

high HR, regular rhythm, narrow QRS.

Question 532

Acute Mx of SVT?

Answer 532

• vagal manoeuvres eg. valsalva manoeuvre (eg. flow into empty syringe) or carotid sinus massage.
• fluids (both fluids and vagal normally work for sinus tachy)
• IV adenosine (usually needed)
• electrical cardioversion

Question 533

Dose of adenosine in SVT?

Answer 533

rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg

Question 534

Who is adenosine for SVT contraindicated in?

Answer 534

asthmatics- use veramil

Question 535

Prevention of SVT?

Answer 535

BB
radio-frequency ablation

Question 536

Torsades de pointes (rhythm strip can look like ribon- ‘twisting of the points’) is what?

Answer 536

Form of polymorphic ventricular tachy associated with long QT interval

Question 537

Why can torsades de pointes lead to sudden death?

Answer 537

can deteriorate into V Fib

Question 538

Causes of long QT interval?

Answer 538

• congenital
• drugs
• electrolyte: hypocal; hypokal; hypomag
• myocarditis
• hypothermia
• subarachnoid haemorrhage

Question 539

Drugs that can cause long QT interval?

Answer 539

• antiarryhtmics eg. amiodarone
• tricyclic antidep
• antipyschotics
• chloroquine
• terfenadine
• erythromycin (macrolides)

Question 540

Mx of torsades de pointes?

Answer 540

IV magnesium sulphate

Question 541

Ventricular tachycardia?

Answer 541

broad complex tachy originating from ventricular ectopic focus

Question 542

V tach can deteriorate to what?

Answer 542

V fib so need urgent Mx

Question 543

2 types of V tach?

Answer 543

• monomorphic: commonly caused by MI. QRS complexes look same.
• polymorphic: eg. torsades de pointes. QRS complexes look different

Question 544

Mx of V tach?

Answer 544

1) pulse? if no then ALS + defib +/- epi & amio
2) if pulse= adenosine
3) if doesn’t work then try other antiarrythmics: procainomide, amiodarone, lidocaine
4) prepare for synchronised electrical cardioversion

Question 545

What drug should not be used in V tach?

Answer 545

Verapamil

Question 546

Shockable rhythms?

Answer 546

Ventricular fibrillation and pulseless ventricular
tachycardia

Question 547

Non-shockable rhythms?

Answer 547

pulseless electrical activity and asystole

Question 548

Most dangerous rhythms?

Answer 548

V tach and V fib

Question 549

Adult advanced life support?

Answer 549

1) CPR 30:2 (100-120/min), attach defib
2) assess rhythm

3) shockable: 1 shock, immediately resume CPR for 2mins
3) non-shockable: continue CPR

4) whilst doing this obtain IV or intraosseous access
5) give adrenaline 1mg every 3-5mins and amiodarone 300mg after 3 shocks and then 150mg after 5 shocks

Question 550

Reversible causes of cardiac arrest?

Answer 550

H.ypoxia
H.ypovolaemia
H.yperkal, hypokal, hypogly, hypocal
H.+ (acidaemia)
H.ypothermia

T.hrombosis (coronary or pulmomary
T.ension pneumothorax
T.amponade (cardiac)
T.oxins

Question 551

How old is an infant vs a child?

Answer 551

Infant= <1yr
Child= 1yr-puberty

Question 552

Child advanced life support?

Answer 552

1) 5 rescue breaths
2) check femoral pulse
3) 15:2 (chest compressions 100-120/min)

Question 553

Depth for chest compressions?

Answer 553

Lower half of sternum by at least 1/3 of anterior-posterior dimension of chest (4cm for infant, 5cm for child/adult)

Question 554

Position for chest compressions in adults & children and infants?

Answer 554

• adults & children= lower half of sternum
• infants: 2 thumb encircling technique (on lower 1/3 of sternum)

Question 555

Features of pulmonary oedema/HF on CXR?

Answer 555

A.lveolar and interstitial oedema (bat’s wing appearance)
B. Kerley B-lines
C.ardiomegaly
D.ilated upper lobe vessels (increased blood flow to superior part of lung)
E.ffusion (pulmonary)

Question 556

What do Kerley B lines represent?

Answer 556

Expansion of interstitial space by fluid

Question 557

Symptoms of heart failure?

Answer 557

S.hortness of breath
O.rthopnea
F.atigue
A.nkle swelling

P.ulmonary oedema
C.old peripheries

cough worse at night, pink/frothy sputum; cardiac wheeze; cardiac cachexia

Question 558

Signs of heart failure?

Answer 558

elevated jugular venous pressure, bibasal crepitations and peripheral oedema.

Question 559

What causes heart failure?

Answer 559

structural and/or functional abnormality that produces raised intracardiac pressures and/or inadequate cardiac ouput at rest and/or at exercise

Question 560

CP of right sided HF

Answer 560

raised JVP, peripheral oedema (ankle/sacral), hepatomegaly, weight gain due to fluid retention, anorexia (cardiac cachexia)

Question 561

CP of left sided HF

Answer 561

pulmonary oedema: dyspnoea, cough, orthopnoea, paraoxysmal nocturnal dyspnoea, bibasal fine crackles

Question 562

Heart failure is classified into what 3 main categories?

Answer 562

1) reduced ejection fraction
2) midly reduced EF
3) preserved EF

Question 563

What is the New York Heart Association functional classification?

Answer 563

symptoms of heart failure are classified according to severity

Question 564

HF is usually caused by what?

Answer 564

myocardial dyfunction, systolic or diastolic or move

most common underlying pathophysiology= coronary artery disease

Question 565

Cx of HF?

Answer 565

arrhythmias, depression, cachexia, CKD, sexual dysfunction, sudden cardiac death

Question 566

Steps to follow if HF is suspected clinically? (Ix)

Answer 566

• N-terminal pro b-type natriuretic peptide (NT-proBNP)
• if normal then HF unlikely, if raised then refer for specialist assessment and echo

Question 567

What levels should NT-pro-BNP be to be referred for specialist assessment and transthoracic echo if suspected HF?

Answer 567

> 2000ng/L then urgent within 2w

400-2000 then refer within 6w

Question 568

Ix for all people with suspected HF

Answer 568

• NT-pro-BNP (?may need transthoracic echo)
• 12 lead ECG
• Loop diuretic for symptom relief whilst waiting for assessment
  -? CXR, bloods, urine dip (protein and blood), peak flow

Question 569

Mx for HF with reduced ejection fraction?

Answer 569

• diuretic if fluid overload
• ACE inhibitor AND BB
• • mineralcorticoid receptor antagonist (MRA eg. spironolactone) if still symptomatic
• specialist advice if still symptomatic

Question 570

Mx for HF with mildly reduced EF?

Answer 570

• loop diuretic if fluid overload
• consider ACE, BB and maybe MRA eg. spirinolactone

Question 571

Mx for HF with preserved ejection fraction?

Answer 571

low-medium dose loop diuretic if needed and refer if no response. Manage cormorbities eg. HTN, AF, IHD, DM

Question 572

What to give all pts with confirmed HF?

Answer 572

• consider antiplatelet and statin
• offer personalised exercise based cardiac rehab programme
• lifestyle advice
• assess nutritional status
• screen for depression and anxiety
• offer appropriate vaccinations (influenza and pneumococcol)

Question 573

RFs for HF?

Answer 573

Coronary artery disease, previous MI, HTN, AF, DM, drugs & alcohol, FHx sudden cardiac death <40yrs or HF

Question 574

What should you examine for in pt with suspected HF?

Answer 574

1) tachy (>100bpm) and pulse rhythm
2) laterally displaced apex beat, murmurs, added heart sounds (gallop rhythm)
3) HTN
4) increased JVP
5) enlarged liver
6) resp signs: tachypnoea, basal crep, pleural effusions
7) leg or sacrum oedema, ascites
8) obesity

Question 575

What is a common this for pts with HF to do?

Answer 575

sleep with lots of pillows (orthopnea)

Question 576

Dose of loop diuretic for symptomatic relief for pts with HF?

Answer 576

furosemide 20-40mg daily

Question 577

Natriuretic peptide levels may be reduced by what?

Answer 577

BMI >35
African-Caribbean origin
Drugs eg. diuretics, ACE, BB, ARB, mineralcortioid receptor antagonists eg. spironolactone

Question 578

Natriuretic peptide levels may be elevated by what?

Answer 578

> 70yrs; LV hypertrophy, MI, tachy; RV overload; hypoxia; pulmonary HTN; pulmonary embolism; CKD; sepsis; COPD; DM; liver cirrhosis

Question 579

Advice to give pt who has HF and is acutely unwell?

Answer 579

Maintain fluid intake and stop ACE, BB, MRA until eating and drinking normally

Question 580

Specialist Mx of HF of reduced EF and ACE+BB+MRA not worked?

Answer 580

Either of….
1) <35% EF replace ACI (or ARB) with sacubitril
2) + ivabradine for sinus rhythm with HR >75 and EF <35%
3) + hydralazine and nitrate (esp if African-C descent)
4) digoxin for HF with sinus rhythm to improve symptoms

5) may need cardiac resynchronisation therapy or insertion of ICD (implantable cardioverter defib)

Question 581

Ramipril initial and target dose for HF?

Answer 581

2.5mg once a day
then target of 5mg twice a day or 10mg once

Question 582

Initial and target dose of bisoprolol for HF?

Answer 582

1.25mg once a day
then target 10mg once a day

(1.25-2.5 to 3.75-5 week 1; 5mg od 4w then 7.5 od for 4w then 10mg)

Question 583

Dose of furosemide for HF?

Answer 583

20-40mg

Question 584

When is b-type natriuretic peptide (BNP) or NTproBNP produced by the heart?

Answer 584

in response to strain

Question 585

Why is exercise training good for HF?

Answer 585

improves symptoms but not hospital/mortality

Question 586

When is cardiac resynchronisation therapy used for pts with HF?

Answer 586

• HF and wide QRS
• biventricular pacing
• improved CP and reduces hospitalisation in NYHA class III pts

Question 587

How many classes in NYHA classication?

Answer 587

4

Question 588

NYHA Class I

Answer 588

no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

Question 589

NYHA Class II

Answer 589

mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

Question 590

NYHA Class III

Answer 590

moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

Question 591

NYHA Class IV

Answer 591

severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Question 592

What is acute heart failure (AHF)?

Answer 592

sudden onset or worsening of the symptoms of HF

may be present with or without Hx of pre-existing HF

Question 593

What is de-novo AHF?

Answer 593

acute HF without a past history of HF

Question 594

What is decompensated AHF?

Answer 594

background history of HF

Question 595

AHF is usually caused by a reduced…

Answer 595

cardiac output that results from functional or structural abnormality

Question 596

Causes of de-novo AHF?

Answer 596

• increased cardiac filling pressures and myocardial dysfunction as a result of ischaemia -> reduced cardiac output and so hypoperfusion -> pulmonary oedema
• less common: viral myopathy, toxins, valve dysfunction

Question 597

Causes of decompensated HF?

Answer 597

• acute coronary syndrome
• HTN crisis
• acute arrhythmia
• valvular disease

Question 598

Patients with HF are broadly characterised into what groups based on what they present with?

Answer 598

• with or without hypoperfusion
• with or without fluid congestion

Question 599

Symptoms of AHF?

Answer 599

breathlessness, reduced exercise tolerance, oedema, fatigue

Question 600

Signs of AHF?

Answer 600

cyanosis, tachy, elevated JVP, displaced apex beat, bibasal crackles (maybe a wheeze), S3 heart sound

Question 602

over 90% pts with AHF have a normal or increased…

Answer 602

BP

Question 603

Ix for AHF

Answer 603

• BNP/NT-pro-BNO
• CXR
• bloods (?infection, electrolyte, anaemia)
• echo

Question 604

Acute Mx for HF

Answer 604

1) IV loop diuretic eg. furosemide
2) O2
3) Do not routinely offer nitrates, opiates, inotropes or vasopressors
4) CPAP if resp failure

Question 605

When to offer nitrates in acute Mx of HF?

Answer 605

pt with concomitant MI, severe HTN or regurgitant aortic/mitral valve

Question 606

When to offer inotropes or vasopressors in the acute Mx of HF?

Answer 606

pts who have potentially reversible cardiogenic shock
eg. dobutamine (inotrope) and norepinephrine (vasopressor)

Question 607

When should BB only be stopped in the acute Mx of HF?

Answer 607

if HR <50, second or third degree AV block or shock

Question 608

HF with reduced ejection fraction level?

Answer 608

<35-40% (measured with echo)

Question 609

HF with rEF typically has what type of dysfunction?

Answer 609

systolic (impaired myocardial contraction during systole)

Question 610

HF with pEF typically has what type of dysfunction?

Answer 610

diastolic (impaired V filling during diastole)

Question 611

Causes of systolic dysfunction (as so HF-rEF)?

Answer 611

IHD
Dilated cardiomyopathy
Myocarditis
Arrhythmias

Question 612

Causes of diastolic dysfunction (as so HF-pEF)?

Answer 612

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

Question 613

Most urgent symptom of acute HF?

Answer 613

LV failure causing pulmonary oedema

Question 614

HR-rEF and HR-pEF typically develop what sided HF?

Answer 614

Left

Question 615

Why may HR-rEF and HR-pEF develop left-sided HF?

Answer 615

increased LV afterload eg. arterial HTN or aortic stenosis; or increased LV preload eg. aortic regurg resulting in backflow to LV

Question 616

What causes right sided HF?

Answer 616

increased RV afterload (eg. pulmonary HTN) or increased RV preload (eg. tricuspid regurg)

Question 617

Left and right sided HF can be used to describe the consequences of HF ie. the backward failure of output of…

Answer 617

either RV or LV

Question 618

What is high-output HF?

Answer 618

‘normal’ heart is unable to pump enough blood to meet metabolic needs of body

Question 619

Causes of high-output HF?

Answer 619

anaemia, AV malformation, Paget’s, pregnancy, thyrotoxicosis, thiamine def

Question 620

Angina?

Answer 620

chest pain/constricting discomfort caused by insufficient blood supply to myocardium

Question 621

causes of angina?

Answer 621

CAD, valvular disease, hypertrophic obstructive cardiomyopathy or HTN heart disease

Question 622

Stable angina?

Answer 622

occurs predictably with physical exertion or emotional stress and is relieved within mins of rest or with a dose of sublingual glyceryl trinitrate

Question 623

Unstable angina?

Answer 623

New (usually <24hrs) onset angina or abrupt deterioration in previously stable angina, often occurring at rest. Requires immediate admission/referral to hospital.

Question 624

Mx of stable angina?

Answer 624

• lifestyle advice
• Sublingual glyceryl trinitrate (GTN) for rapid relief
  + a BB or CCB (first line)
• 2nd: long-acting nitrate eg. isosorbide mononitrate
• poor control then add another drug from different class, if still poor then referral to cardio

Question 625

Drugs for secondary prevention of CV events for pts with angina?

Answer 625

low dose aspirin 75mg daily
ACE inhibitor
- Mx for lipid modification and HTN if appropriate

Question 626

Hospital admission is recommended for people with possible unstable angina presenting with what symptoms?

Answer 626

• pain at rest (may be at night)
• pain on minimal exertion
• angina rapidly progressing despite medical Mx

Question 627

Typical stable angina CP?

Answer 627

constricting discomfort in chest, neck, shoulders, jaw or arms + precipitated by exercise + relieved by rest or GTN within 5 mins

Question 628

Atypical angina?

Answer 628

2/3 stable angina symptoms + GI discomfort +/or SOB +/or nausea

Question 629

Factors that make diagnosis of stable angina more likely?

Answer 629

age, male, CVD RFs, Hx of coronary artery disease eg. previous MI, coronary revascularisation

Question 630

Factors that make diagnosis of stable angina less likely?

Answer 630

continuous or prolonged pain, unrelated to activity; brought on my breathing; associated with dizziness, palpitations, tingling or diff swallowing

Question 631

Ix for angina?

Answer 631

Clinical
Resting ECG

Question 632

Hypertension?

Answer 632

Persistently raised arterial BP

Question 633

Hypertension increases the risk of what conditions?

Answer 633

HF, CAD, stroke, CKD, peripheral arterial disease, vascular dementia

Question 634

2 types of HTN?

Answer 634

primary and secondary

Question 635

Primary HTN (essential HTN)?

Answer 635

90% of pts.
NO identifiable cause.

Question 636

Secondary HTN?

Answer 636

has known underlying cause eg. renal, endocrine, or vascular disorder or use of certain drugs

Question 637

When should HTN be suspected?

Answer 637

Clinic SBP >=140mmHg or DBP >=90

Question 638

Ix for HTN?

Answer 638

• Clinic BP: if 140/90 to 179/119 offer ambulatory BP monitoring (ABPM) to confirm diagnosis. If unable offer home blood pressure monitoring (HBPM).
• If clinic 180/120 or higher= same day referral if indicated or Ix for target organ damage. Start antihypertensive Mx immediately.

Question 639

What should be done whilst waiting for confirmation of diagnosis of HTN?

Answer 639

Ix for target organ damage and 2 causes of HTN.
Assess CV risk.

Question 640

Classification of HTN (according to severity)?

Answer 640

• Stage 1= clinic BP 140/90 to 159/99 AND ABPM or HBPM average 135/85 to 149/94
• Stage 2= clinic 160/100 to 179/119 AND ABPM/HBPM 150/95 or higher
• Stage 3= clinic SBP 180+ OR clinic DBP 120+

Question 641

Accelerated/malignant HTN?

Answer 641

severe increase in BP to 180/120 or higher (ofter >220/120) with signs of retinal haemorrhage and/or papilloedema (swelling of optic nerve)

Question 642

White-coat HTN?

Answer 642

BP unusually raised when measured during clinic but normal in other ‘non-threatening’ situations eg. home. Suspect if discrepancy of more than 20/10mmHg between clinic and avergae ABPM/HBPM readings.

Question 643

HTN referral for same day specialist assessment should be arranged when?

Answer 643

• clinic BP 180/120+ with signs of retinal haemorrhage/papilloedema OR life-threatening symptoms
• suspected phaeochromocytoma

Question 644

Life-threatening symptoms for pt with HTN?

Answer 644

new onset confusion, chest pain, signs of HF, AKI

Question 645

CP for suspected phaeochromocytoma?

Answer 645

labile or postural hypotension, headache, palpitations, pallor, abdo pain or diaphoresis

Question 646

Overall things the Mx of HTN includes?

Answer 646

• lifestyle advice
• antihypertensive drug Mx
• ?statin
• monitor

Question 647

When should pts with HTN be reviewed?

Answer 647

Annually= BP, review meds, discuss lifestyle, symptoms

Question 648

Target BP for <80yrs?

Answer 648

clinic= <140/90
ABPM/HBPM= <135/85

Question 649

Target BP for 80yrs+?

Answer 649

clinic= <150/90
ABPM/HBPM= <145/85

Question 650

BP target for someone with postural hypertension?

Answer 650

Base on standing BP

Question 651

How to measure BP in suspected HTN?

Answer 651

Relaxed setting, person quiet and seated with arm outstretched and supported.
Both arms.
If diff in reading between arms >15 then repeat. If still different use higher reading/

Question 652

When might automated BP devices not be accurate?

Answer 652

If pulse irregularity eg. AF so measure BP manually using direct auscultation over brachial artery if pulse irregular

Question 653

Measure BP for pt with suspected hypotension?

Answer 653

Measure seated/supine then again when standing for >1min before measurement. If SBP falls by 20+ when standing, measure subsequent BP with person standing

Question 654

What if BP measured in clinic 140/90 or higher?

Answer 654

Take second measurement and record the lower of the 2

Question 655

How to use HBPM?

Answer 655

For each BP reading: take 2, 1 min apart whilst seated. Record twice daily (morning and evening) for >4days (ideally 7). Discard first day measurements and use average of all values to confirm HTN.

Question 656

When to confirm diagnosis of HTN?

Answer 656

Clinic BP 140/90 or higher AND ABPM/HBPM average of 135/85 or higher

Question 657

When to suspect masked HTN?

Answer 657

If clinic BP normal (<140/90) but BP are higher using ABPM or HBPM

Question 658

When to suspect secondary HTN?

Answer 658

Pts <40yrs or those with accelerated HTN or if suspicious of underlying cause eg. meds

Question 659

What if HTN is not diagnosed?

Answer 659

• ?evidence of target organ damage
• if not then measure clinic BP every 5yrs after or more frequently if clinic BP close to 140/90

Question 660

How to Ix for target organ damage in pt with HTN?

Answer 660

• haematuria
• urine albumin:creatinine ratio (?protein in urine)
• HbA1c
• electrolytes, creatine and eGFR (?CKD)
• examine fundi (HTN retinopathy)
• ECG

specialist Ix if target organ damage or 2 cause of HTN

Question 661

Assess CV risk in pt with HTN?

Answer 661

• serum total cholesterol and HDL cholesterol
• QRISK

Question 662

HTN Mx if <55yrs, with or without DMT2?

Answer 662

1) ACEi or ARB
2) ACEi or ARB + CCB or diuretic
3) ACEI or ARB + CCB + thiazide-like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice

Question 663

HTN Mx if 55yrs or over, Black-African or African-Caribbean origin, without DMT2?

Answer 663

1) CCB
2) CCB + ACEi (or ARB) OR diuretic
3) ACEi/ARB + CCB + thiazide like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice

Question 664

When should you use an ARB over an ACEi in HTN MX?

Answer 664

If ACEi side effects eg. cough not tolerated

Question 665

When to use thiazide like diuretic over CCB in HTN Mx?

Answer 665

If not tolerated eg. because of oedema

Question 666

When to use CCB first line in HTN Mx over ACEi/ARB?

Answer 666

if 55 yrs or over and DO NOT have DMT2
or
black African or African-Caribbean origin and don’t have DMT2

Question 667

What to do in HTN Mx if have diabetes and are black African?

Answer 667

use ARB in perference to ACE

Question 668

What to do in HTN Mx before offering another drug in addition to others?

Answer 668

review and ensure taking optimal tolerated doses; discuss adherence

Question 669

ACEi example and dose for HTN Mx?

Answer 669

Ramipril

staring dose= 1.25-2.5mg OD
maintenance= 2.5-10mg OD
max= 10mg OD

Question 670

ARB example and dose of HTN Mx?

Answer 670

Candesartan

starting= 8mg OD
maintenance= 8mg OD
max= 32mg OD

Question 671

Thiazide-like diuretic example and dose for HTN Mx?

Answer 671

Indapamide

2.5mg in morning (immediate release) or 1.5mg (modified)

Question 672

CCB example and dose for HTN Mx?

Answer 672

Amlodipine

start= 5mg OD
maintenance= 5-10mg OD
max= 10mg OD

Question 673

Spironolactone dose for HTN Mx?

Answer 673

25mg OD with food

Question 674

BB example and dose for HTN Mx (last line)?

Answer 674

Bisoprolol

start= 5mg OD in morning
maintenance= 10mg OD
max= 20mg OD

Question 675

If pt BP is very high eg. >200/120mmHg what symptoms might they get? (HTN typically asymptomatic)

Answer 675

headaches, visual disturbance, seizures

Question 676

Why do you go ECG, fundoscopy and urine dip on pt with newly diagnosed HTN?

Answer 676

ensure don’t have end-organ damage.
eg. F= HTN retinopathy
UD= renal disease (cause or consequence of HTN)
ECG= LV hypertrophy or IHD

Question 677

How to measure BP in children?

Answer 677

• correct cuff size is 2/3 length of upper arm
• 4th Korotkoff sound used to measure DBP until adolescence, then 5th Korotkoff sound can be used
• compare results with graph of normal values for age

Question 678

What is the most common cause of HTN in younger children?

Answer 678

secondary HTN eg. renal parenchymal disease

Question 679

Causes of HTN in children?

Answer 679

• renal parenchymal disease
• renal vascular disease
• coarctation of aorta
• phaeochromocytoma
• congenital adrenal hyperplasia
• as child is older: essential/primary HTN

Question 680

What drugs can cause HTN?

Answer 680

steroids, NSAIDs, COCP, monoamine oxidase inhibitors

Question 681

Most common cause of secondary HTN?

Answer 681

Primary hyperaldosteronism (incl. Conn’s)

Question 682

Renal causes of HTN?

Answer 682

glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis

Question 683

Endocrine causes of HTN?

Answer 683

• primary hyperaldosteronism
• phaeochromocytoma
• Cushing’s syndrome
• Liddle’s syndrome
• congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
• acromegaly

Question 684

Other causes of HTN?

Answer 684

pregnancy
coarctaation of aorta

Question 685

Strongest RF for developing infective endocarditis?

Answer 685

previous episode of endocarditis

Question 686

What valve is most commonly affected in endocarditis?

Answer 686

mitral

Question 687

What types of pts are typically affected by endocarditis?

Answer 687

• prev normal valves
• rheumatic valve disease
• prosthetic valves
• IVDUs
• congenital heart defects
• recent piercings

Question 688

Fever and new murmur

Answer 688

infective endocarditis likely

Question 689

Causes of infective endocarditis?

Answer 689

staph aureus (most common)
strep viridans
staph epidermidis

Question 690

poor oral hygiene/recent dental surgery- cause of IE?

Answer 690

strep viridans

Question 691

Murmur in IE caused by strep viridans?

Answer 691

mitral/aortic regurg

Question 692

Infective endocarditis in IVDU or acute presentation

Answer 692

staph aureus

Question 693

Murmur in IE caused by staph aureus

Answer 693

Tricuspid (splitting of 2nd heart sound)

Question 694

Infective endocarditis following prosthetic valve surgery

Answer 694

staph epidermidis

Question 695

Streptococcus bovis (s. gallolyticus) that can cause infective endocarditis is associated with what?

Answer 695

colorectal cancer

Question 696

Non-infective causes of endocarditis?

Answer 696

SLE
malignancy (marantic endo)

Question 697

Culture negative causes of infective endocarditis?

Answer 697

prior Abx therapy
Coxiella burnetii
Bartonella
HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

Question 698

Infective endocarditis?

Answer 698

inflam of endocardium (inner lining of heart) and valves primarily caused by bacteria

Question 699

Criteria to diagnose infective endocarditis?

Answer 699

Modified Duke Criteria

Question 700

When is infective endocarditis diagnosed using the Modified Duke criteria? (4)

Answer 700

1) pathological criteria positive, or

2) 2 major criteria, or

3) 1 major and 3 minor, or

4) 5 minor

Question 701

Infective endocarditis: what is a positive pathological criteria on Modified Duke?

Answer 701

1) microorganisms in a vegetation on histology (autopsy or surgery)
OR
2) Pathologic legions on histology of vegetation or intracardiac abscess

Question 702

Duke Modified Criteria for infective endocarditis: what is included in the major criteria?

Answer 702

1) Typical microorganisms consistent of IE from 2 separate blood cultures taken >12hrs apart

2) Evidence of endocardial involv. on ECHO

Question 703

Duke Modified Criteria for infective endocarditis: what is included in the minor criteria?

Answer 703

1) Predisposing heart condition or IVDU

2) Fever >38

3) Vascular phenomena: conjunctival haemorrhages, Janeway’s lesions, intracranial haemorrhage, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, splinter H

4) Immunologic phenomena: Osler’s nodes, Roth’s spots, Glomerulonephritis, rheumatoid factor

5) Microbio evidence: +ve blood culture that doesn’t meet major criteria or serological evidence of active infection consistent with IE

Question 704

Ix for infective endocarditis?

Answer 704

• Blood cultures (1st)
• Trans-oesphageal ECHO (vegetation)
• ECG: prolonged PR

Question 705

Infective endocarditis CP?

Answer 705

F.ever >38
R.oth spots
O.cler’s nodes= fingertips, painful
M.urmur

J.aneway lesions: palm, painless
A.naemia
N.ail bed splinter haemorrhages
E.mboli

Predisposing heart condition, IVDU, recent dental surgery

Question 706

Poor prognostic factors of infective endocarditis?

Answer 706

• staph aureus
• prosthetic valve
• culture -ve endocarditis
• low complement levels

Question 707

Mortality of infective endocarditis according to organism?

Answer 707

staphylococci - 30%
bowel organisms - 15%
streptococci - 5%

Question 708

Summary of Mx of infective endocarditis?

Answer 708

• inital blind Abx therapy
• then specific Abx therapy
• ?surgery

Question 709

Mx of infective endocarditis: inital blind Abx therapy (empirical)? What is allergic/MRSA/sepsis? What if prosthetic valve?

Answer 709

• Amoxicillin, consider + low dose gentamicin
• MRSA, severe sepsis or penicillin allergic: vancomycin + low dose gentamicin
• If prosthetic valve: vancomycin + rifampicin + low dose gentamicin

Question 710

Specific Abx therapy for infective endocarditis if native valve (normal) caused by staphlococci? Allergic/MRSA?

Answer 710

Flucloxacillin

Allergic/MRSA= vancomycin + rifampicin

Question 711

Specific Abx therapy for infective endocarditis if prosthetic valve caused by staphlococci? Allergic/MRSA?

Answer 711

Flucloxacillin + rifampicin + low-dose gentamicin

Allergic/MRSA=
vancomycin + rifampicin + low-dose gentamicin

Question 712

Specific Abx therapy for infective endocarditis if caused by fully-sensitive strep (eg. viridans)? Allergic?

Answer 712

Benzylpenicillin

Allergic= vancomycin + low-dose gentamicin

Question 713

Specific Abx therapy for infective endocarditis if caused by less sensitive strep? Allergic?

Answer 713

Benzylpenicillin + low-dose gentamicin

Allergic= vancomycin + low-dose gentamicin

Question 714

Typical Abx if allergic to penicillin or MRSA (eg. if use flucloxacillin)?

Answer 714

vancomycin

Question 715

Indications for surgery in infective endocarditis?

Answer 715

• severe valvular incompetence
• aortic abscess
• infections resistant to Abx
• funal infections
• recurrent emboli after Abx

Question 716

Pts with what cardiac conditions are at incresed risk of developing infective endocarditis?

Answer 716

• acquired valvular heart disease with stenosis or regurg
• hypertrophic cardiomyopathy
• previous IE
• structural congential heart disease
• valve replacement

Question 717

Advice to give pts who are at increased risk of IE?

Answer 717

• benefits and risks of Abx prophylaxis and why it’s no longer recommeneded
• importance of good oral health
• CP of IE
• risks of invasive procedures incl. non medical eg. piercing or tattoos

Question 718

Is Abx prophylaxis for IE routinely recommended?

Answer 718

No

Question 719

What should pts who take standard release isosorbide mononitrate for stable angina Mx do to prevent development of nitrate tolerance and reduced efficacy?

Answer 719

use asymmetric dosing interval to maintain a daily nitrate-free time of 10-14hrs.

(not seen in pts who take modified release)

Question 720

Another name for stable angina?

Answer 720

Angina pectoris

Question 721

Causes of mitral valve prolapse?

Answer 721

usually idiopathic but can be associated with other conditions and CVD

Question 722

Mitral valve prolapse? (Barlow syndrome)

Answer 722

the cusps of the mitral valve become enlarged or strecth and these bulge (prolapse) into LA as heart contracts

Usually doesn’t require Mx unless causes severe regurg

Question 723

Mitral valve prolapse associations?

Answer 723

congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

Question 724

Features of mitral valve prolapse?

Answer 724

• atypical chest pain/palpitations
• mid-systolic click (later if pt squatting)
• late systolic murmur (longer if pt standing)

Question 725

Cx of mitral valve prolapse?

Answer 725

mitral regurg, arrhythmias (long QT), emboli, sudden death

Question 726

Myocarditis?

Answer 726

Inflamm of myocardium

Question 727

Consider what is a young pt with acute chest pain?

Answer 727

myocarditis

Question 728

Causes of myocarditis?

Answer 728

• viral: coxsackie B, HIV
• bacteria: diptheria, clostridia
• spirochaetes: Lyme disease
• protozoa: Chagas’ disease, toxoplasmosis
• autoimmune
• drugs: doxorubicin

Question 729

CP of myocarditis?

Answer 729

• usually young pt with acute Hx
• chest pain
• dyspnoea
• arrhythmias

Question 730

Ix for myocarditis?

Answer 730

• Bloods= Increased: CRP & ESR, cardiac enzymes and BNP, elevated troponin
• ECG

Question 731

ECG findings in myocarditis?

Answer 731

• tachycardia
• arrhythmias
• ST/T wave changes incl ST elevation and T wave inversion

Question 732

Mx for myocarditis?

Answer 732

• TUC eg. Abx if bacterial causes
• supportive treatment eg. of HF or arrhythmias

Question 733

Cx of myocarditis?

Answer 733

• HF
• arrhythmia, possibly leading to sudden death
• dilated cardiomyopathy: usually a late complication

Question 734

Classic features of cardiac tamponade?

Answer 734

Beck’s triad: hypotension, muffled heart sounds, raised JVP

Question 735

CP of cardiac tamponade?

Answer 735

• Beck’s triad
• dyspnoea
• tachycardia
• absent Y descent on JVP (due to limited RV filling)
• pulsus paradoxus
• Kussmaul’s sign rare

Question 736

ECG feature of cardiac tamponade?

Answer 736

electrical alternans (alternating QRS amplitude seen in any or all leads with no other changes to conduction pathways)

Question 737

Pulsus paradoxus?

Answer 737

abnormally large drop in BP during inspiration

Question 738

Kussmaul’s sign?

Answer 738

Paradoxical increase in JVP that occurs during inspiration. Seen in cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy

Question 739

What does an absent Y descent mean?

Answer 739

when filling of RV is impaired following opening of tricuspid valve

eg. in cardiac tamponade:
TAMponade=TAMpaX (no Y)

Question 740

Ix for cardiac tamponade?

Answer 740

transthoracic echo and ECG

Question 741

What does X and Y mean in JVP?

Answer 741

X descent= RA relaxation
Y descent= RV filling (tricuspid opens)

Question 742

Difference in features between cardiac tamponade and constrictive pericarditis?

Answer 742

CT= JVP absent Y descent; pulsus paradoxus present; Kussmaul’s sign rare

CP= X + Y present; absent pulsus paradoxus; present Kussmaul’s sign; pericardial calfication on CXR

Question 743

Causes of constrictive pericarditis?

Answer 743

any cause of pericarditis, particularly TB

Question 744

Constrictive pericarditis?

Answer 744

Granulation tissue formation in pericardium results in loss of pericardial elasticity leading to restriction in V filling

Question 745

CP of constrictive pericarditis?

Answer 745

• dyspnoea
• RHF: elevated JVP, ascites, oedema, hepatomegaly
• JVP shows X and Y descent
• pericardial knock (loud S3)
• Positive Kussmaul’s sign

Question 746

Ix for constrictive pericarditis?

Answer 746

CXR: pericardial calcification

Question 747

Mx for constrictive pericarditis?

Answer 747

NSAIDs, diuretics
Only definitive Mx= pericardiectomy but use in caution if mild disease as high mortality

Question 748

Causes of pericardial effusion?

Answer 748

infectious pericarditis: viral, tuberculosis, pyogenic spread from septicaemia and pneumonia
uraemia
idiopathic
post myocardial infarction (including Dressler’s syndrome)
malignancy
heart failure
nephrotic syndrome
hypothyroidism
trauma

Question 749

Pericardial effusion can be made of what?

Answer 749

Transudates (low protein content)
Exudates (associated with inflammation)
Blood
Pus
Gas (associated with bacterial infections)

Question 750

Pericardial effusion?

Answer 750

XS fluid collects within pericardial sac; can be cute or chronic; can fill entire pericardial cavity or only a localised section

Question 751

Pericardial effusion: transudative effusion?

Answer 751

Results from increased venous pressure that can reduce drainage from pericardial cavity. May occur in congestive HF and pulmonary HTN.

Question 752

Pericardial effusion: exudative effusion?

Answer 752

after any inflam process affecting pericardium (pericarditis) eg. infection, autoimmune, trauma, malignancy, methotrexate

Question 753

Rupture of heart or aorta can cause bleeding into the pericardial cavity, resulting in rapid onset cardiac tamponade- rupture may be due to what?

Answer 753

MI, trauma or aortic dissection type A

Question 754

CP of pericardial effusion?

Answer 754

chronic ones may be asymptomatic until pressure rises.

• chest pain, SOB, fullness in chest, orthopnoea
• quiet HS, pulsus paradoxus, hypotension, raised JVP, fever & pericardial rub (with pericarditis)

Question 755

Pericardial effusion may compress surrounding structures causing other symptoms like….

Answer 755

• Phrenic nerve compression= hiccups
• Oseophageal= dysphagia
• Recurrent laryngeal nerve= hoarse voice

Question 756

Ix for pericardial effusion?

Answer 756

• ECHO (gold & 1st)
• fluid analysis: underlying cause eg. protein content, bacterial culture, viral PCR, cytology & tumour markers

Question 757

Mx for pericardial effusion?

Answer 757

• TUC eg. inflamm: NSAIDs and colchicine
• Draining: needle pericardiocentesis

Question 758

Pericardial window?

Answer 758

surgical procedure where portion of pericardium removed creating a ‘window’/fistula to allow fluid to drain from pericardial cavity to pleural carvity/peritoneal cavity

Question 759

Membrane that surrounds the heart?

Answer 759

Pericardium/pericardial sac

Question 760

What is the pericardium made from?

Answer 760

2 layers with small amount of fluid in between (<50ml) providing lubrication to allow heart to beat without friction. These layers separate heart from rest of contents of mediastinum.

Question 761

What is between the 2 layers of the pericardium?

Answer 761

‘potenital space’ called pericardial cavity, layers usually touch eachother which is my it is only a potential space. Small amount of fluid.

Question 762

Potential space of pericardial cavity fills with fluid?

Answer 762

Pericardial effusion. Creates inward pressure on heart making it more difficult to expand during diastole (filling of heart).

Question 763

What is it called when the pericardial effusion is large enough to raise intra-pericardial pressure?

Answer 763

Cardiac tamponade. Leads to reduced filling of heart during diastole resulting in decreased cardiac output during systole.

Question 764

Transudate?

Answer 764

Fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. Eg. due to increased hydrostatic pressure or decreased oncotic pressure

Question 765

Exudate?

Answer 765

Fluid buildup caused by tissue leakage due to inflammation or local cellular damage.

Question 766

Transudate vs exudate?

Answer 766

Transudate:
- Protein <30g/L
- Clear
- Low cell & protein content
- Causes: HF, liver cirrhosis, nephrotic syndrome

Exudate:
- Protein >30g/L
- Cloudy, yellow or bloody
- High cellular & protein content
- Causes: inflam eg. infections (eg. pneumonia), RA, malginancy

Question 767

Are transudate and exudate both extracellular?

Answer 767

Yes they both accumulate in extracellular space eg. tissues or body cavities outside of cells.

Question 768

Exudate diagnostic criteria?

Answer 768

High protein content (>3 g/dL).
High specific gravity (>1.020).
High LDH (lactate dehydrogenase) levels.

Question 769

Transudate diagnostic criteria?

Answer 769

Low protein content (<3 g/dL).
Low specific gravity (<1.012).
Low LDH levels.

Question 770

Reflex syncope?

Answer 770

Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.

Question 771

Most common cause of syncope?

Answer 771

Reflex syncope

Question 772

Subtypes of reflex syncope subtypes?

Answer 772

• vasovagal (faiting)
• situational: cough, micturition, GI
• carotid sinus syncope

Question 773

Vasovagal (reflex) syncope?

Answer 773

• ‘fainting’
• Typically in sitting or standing position & can be triggered by emotion pain or stress.
• CP: warm/hot or light headed prior
• <1-2mins
• prolonged fatigue/amnesia is usual after regaining consciousness

Question 774

What can occur during uncomplicated vasovagal syncope?

Answer 774

brief myoclonic jerks

Question 775

Carotid sinus syncope?

Answer 775

Type of fainting caused by exaggerated response to stimulation of carotid sinus located in neck. Leads to sudden drop in HR & BP -> reduced blood flow to brain and fainting.
Triggers= tight collars, neck pressure, head movements.
- Diagnosis= carotid sinus massage or tilt table test
- Mx: avoid triggers; severe- pacemaker to regulate HR

Question 776

Signs of tricuspid regurg?

Answer 776

• pan-systolic murmur
• prominent/giant V waves in JVP
• pulsatile hepatomegaly
• left parasternal heave

Question 777

Where is loin pain located?

Answer 777

Between lower ribs and buttocks on either side of the spine

Question 778

Where can loin pain originate?

Answer 778

Kidneys, adrenal glands, parts of colon, MSK components, referred from abdo or pelvic organs

Question 779

Renal capsule, ureter and muscles are supplied with what that transmit pain signals to the CNS?

Answer 779

nociceptors

Question 780

Differential diagnosis for loin pain

Answer 780

• ruptured AAA
• renal colic
• pyleonephritis
• MSK pain
• radiculopathy (compression or inflam of spinal nerve roots may cause referred pain)

Question 781

Ix for loin pain?

Answer 781

identifty life-threatening conditions eg. ruptured AAA; history; physical abdo renal and neuro exam; bloods (FBC, renal function); urinalysis; USS/CT; pain Mx

Question 782

What may make atypical presentation of ACS more likely?

Answer 782

female, elderly, diabetic

Question 783

Differential diagnosis for chest pain?

Answer 783

MI
pneumothorax
PE
pericarditis
dissecting aortic aneurysm
GORD
MSK chest pain
perforated peptic ulcer
shingles
Boerhaaves syndrome

Question 784

Referral criteria for chest pain?

Answer 784

• current or <12hrs AND abnormal ECG= emergency admission
• chest pain 12-72hrs ago= refer for same day hospital assessment
• chest pain >72hrs ago= ECG and toponin then decide

Question 785

Mx for pts in whom stable angina can’t be excluded by clinical assessment alone (eg. symptoms consistent with typical/atypical angina OR ECG changes)?

Answer 785

1st line: CT coronary angiography
2nd line: non-invasive functional imaging (?reversible mycardial ischaemia)
3rd: invasive coronary angiography

Question 786

Examples of non-invasive functional imaging?

Answer 786

• myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
• stress echocardiography or
• first-pass contrast-enhanced magnetic resonance (MR) perfusion or
• MR imaging for stress-induced wall motion abnormalities

Question 787

You can characterise congenital heart disease into what?

Answer 787

Cyanotic and acyanotic

Question 788

Most common causes of acyanotic congential heart disease?

Answer 788

• Ventricular septal defects (VSD) (most common, 30%)
• atrial septal defect (ASD)
• patent ductus arteriosus (PDA)
• coarctation of aorta
• aortic valve stenosis

Question 789

What are more common- VSDs or ASDs?

Answer 789

VSDs but in adults ASDs more common new diagnosis as generally present later

Question 790

Most common causes of cyanotic congenital heart disease?

Answer 790

• tetralogy of Fallot
• transposition of great arteries (TGA)
• tricuspid atresia

Question 791

What is more common- tetralogy of Fallot or TGA?

Answer 791

Fallot but at birth TGA is more common lesion as pts with Fallot’s generally present at around 1-2m

Question 792

The presence of cyanosis in pulmonary valve stenosis depends on what?

Answer 792

the severity and any other coexistent defects

Question 793

When is peripheral cyanosis eg. in hands and feet very common?

Answer 793

1st 24hrs of life and may occur when child is crying or unwell

Question 794

Central cyanosis clinical diagnosis?

Answer 794

conc of reduced Hb in blood >5g/dl

Question 795

What can be used to differentiate cardiac from non-cardiac causes of cyanosis in neonatal period?

Answer 795

Nitrogen washout test (hyperoxia test): infant given 100% O2 for 10mins then ABG taken. A pO2 of <15kPa= cyanotic congenital heart disease

Question 796

Initial Mx of suspected cyanotic congenital heart disease?

Answer 796

supportive care + prostaglandin E1 eg. alprostadil

Question 797

Why is prostaglandin E1 eg. alprostadil used in the inital Mx of suspected cyanotic congenital heart disease?

Answer 797

Used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect.
Acts as a holding measure until a definite diagnosis is made and surgical correction performed.

Question 798

Acrocyanosis?

Answer 798

seen in healthy newborns and refers to cyanosis around the mouth and extremities (eg. hands & feet)

Question 799

How is acrocyanosis differentiated from other causes of peripheral cyanosis with signif pathology?

Answer 799

occurs immediately after birth in health infants; common finding as may persist for 24-48hrs

Question 800

Tetralogy of Fallot (TOF)?

Answer 800

most common cause of cyanotic congenital heart disease

Question 801

When does TOF typically present?

Answer 801

1-2m old, may not be picked up until 6m

Question 802

TOF is a result of what?

Answer 802

anterior malalignment of the aorticopulmonary septum

Question 803

4 characteristic features of TOF?

Answer 803

• ventricular septal defect (VSD)
• RV hypertrophy
• overriding aorta
• pulmonary stenosis

Question 804

what can cause RV outflow tract obstruction?

Answer 804

pulmonary stenosis

Question 805

What is the heart defect- overriding aorta?

Answer 805

where aorta is positioned over both the LV & RV (not just the LV); causes it to override the VSD so that it receives blood from both the LV and RV (oxygen rich AND oxygen poor blood); so reduces amount of O2 body receives

Question 806

What determines the degree of cyanosis and clinical severity in TOF?

Answer 806

severity of pulmonary stenosis (and so RV outflow tract obstruction)

Question 807

CP of TOF?

Answer 807

• cyanosis
• ‘tet’ spells
• tachypnoea
• loss of consciousness

Question 808

what are tet spells in TOF?

Answer 808

infants may develop episodic hypercyanotic tet spells due to near occulasion of RV outflow tract.
may become pale/blue (esp fingers and lips); diff breathing; irritable; loss of consciousness

Question 809

Other features of TOF (shunt? murmur?)?

Answer 809

• causes R-to-L shunt
• ejection systolic murmur due to pulmonary stenosis (VSD doesn’t usually cause murmur)
• right-sided aortic arch in 25% pts

Question 810

In TOF what does CXR and ECG show?

Answer 810

• cxr= boot-shaped heart
• ECG= RV hypertrophy

Question 811

Mx of TOF?

Answer 811

• surgical repair often in 2 parts
• beta-blockers for cyanotic episodes to reduce infundibular spasm

Question 812

Transposition of the great arteries (TGA)?

Answer 812

form of cyanotic congenital heart disease caused by the failure of the aorticopulmonary septum to spiral during septation (aorta and pulmonary artery swap places)

Question 813

Who are at increased risk of TGA?

Answer 813

children of diabetic mothers

Question 814

Basic anatomical changes in TGA?

Answer 814

• aorta leaves RV
• pulmonary trunk leaves LV

Question 815

Clinical features of TGA?

Answer 815

• cyanosis
• tachypnoea
• loud single S2
• prominent RV impulse
• ‘egg-on-side’ appearance on CXR

Question 816

Mx for TGA?

Answer 816

• maintenance of ductus arteriosis with prostaglandins
• definitive Mx= surgical correction

Question 817

Coarctation of the aorta?

Answer 817

congenital narrowing of the descending aorta

Question 818

Association of coarctation of aorta?

Answer 818

Turner’s syndrome.

But is more common in males.

Question 819

Coarctation of aorta associations?

Answer 819

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

Question 820

Features of coarctation of the aorta?

Answer 820

• infancy: HF
• adult: HTN

Question 821

Signs of coarctation of aorta on examination?

Answer 821

• radio-femoral delay
• mid systolic murmur, maximal over the back
• apical click from the aortic valve
• notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Question 822

What causes the first heart sound (S1)?

Answer 822

Closure of mitral and tricuspid valves

Question 823

What causes the second heart sound (S2)?

Answer 823

aortic and pulmonary valve closure

Question 824

S1?

Answer 824

closure of mitral and tricuspid valves

Question 825

What causes soft S1?

Answer 825

if long PR or mitral regurg

Question 826

What causes loud S1?

Answer 826

mitral stenosis

Question 827

S2?

Answer 827

closure of aortic and pulmonary valves

Question 828

What causes a soft S2?

Answer 828

aortic stenosis

Question 829

Is splitting of S2 during inspiration normal?

Answer 829

Yes

Question 830

What is a third heart sound (S3) caused by?

Answer 830

diastolic filling of the ventricle

Question 831

When is a S3 normal?

Answer 831

If <30yrs old (may persistent in women up to 50yrs)

Question 832

What is a gallop rhythm?

Answer 832

when S1 and S2 followed by pathological S3 and/or S4. commonly associated with LV failure

Question 833

When may S3 be heard?

Answer 833

LV failure (eg. dilated cardiomyopathy), constrictive pericarditis and in mitral regurg

Question 834

What is S3 called in constrictive pericarditis?

Answer 834

pericardial knock

Question 835

When may a S4 (fourth heart sound) be heard?

Answer 835

in aortic stenosis, HOCM, HTN

Question 836

What causes S4?

Answer 836

Atrial contraction against stiff ventricle; therefore coincides with P wave on ECG

Question 837

In HOCM a double apical impulse may be felt as a result of a…

Answer 837

palpable S4

Question 838

Site of auscultation for pulmonary valve?

Answer 838

Left 2nd ICP at upper sternal border

Question 839

Site of auscultation for mitral valve?

Answer 839

Left 5th ICP just medical to mid clavicular line

Question 839

Site of auscultation for aortic valve?

Answer 839

Right 2nd ICP at upper sternal border

Question 840

Site of auscultation for tricuspid valve?

Answer 840

Left 4th ICS and lower left sternal border

Question 841

Causes of loud S2?

Answer 841

• HTN: systemic (loud A2) or pulmonary (loud P2)
• hyper dynamic states
• ASD without pulmonary HTN

Question 842

Causes of a soft S2?

Answer 842

Aortic stenosis

Question 843

Causes of a fixed (in the middle) split of S2?

Answer 843

atrial septal defect

Question 844

Causes of a widely split S2?

Answer 844

• deep inspiration
• RBBB
• pulmonary stenosis
• severe mitral regurg

Question 845

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)?

Answer 845

• LBBB
• severe aortic stenosis
• RV pacing
• WPW type B (causes early P2)
• patent ductus arteriosus

Question 846

What does S2 sound like?

Answer 846

Higher pitched and shorter duration than S1. ‘dub’ section of ‘lub-dub’

Question 847

What is S2 split into?

Answer 847

Closure of aortic (A2) and pulmonary (P2) valves at end of V systole

Question 848

When do you hear the components of S2?

Answer 848

• A2 normally slightly before P2, P2 softer except in certain conditions it is more pronounced.
• Normal S2: ‘dub’
• Split S2: NORMAL during INSPIRATION where you can hear A2 and P2 distinctively (lub-d-dub’)

Question 849

What does a split S2 mean?

Answer 849

In normal physiology, occurs during inspiration. The 2 components of S2 can be heard separately due to the delay in P2 (resulting in a split sound ‘d-dub’ A2-P2)

Question 850

When is S2 split normal?

Answer 850

During inspiration- corresponds to A2 and P2. (d-dub)

NOT during expiration- sound be heard as a single sound (dub) and not a split

Question 851

Types of split S2?

Answer 851

• physiological (normal in children and young adults, widens with inspiration and narrows with expiration)
• fixed split S2
• wide split S2
• paradoxical split S2

Question 852

Fixed split of S2?

Answer 852

The split (between A2 and P2) remains constant during both inspiration and expiration.

Question 853

What is associated with a fixed split of S2?

Answer 853

ASD

Question 854

Wide split S2?

Answer 854

the split (sounds of A2 and P2) is wider than normal and persists during inspiration and expiration.

Question 855

What is associated with wide split S2?

Answer 855

RBBB or pulmonary HTN

Question 856

What is a paradoxical split s2?

Answer 856

Split (sounds of A2 and P2) occur during expiration and narrows or disappears during inspiration.

Question 857

What is a paradoxical split S2 associated with?

Answer 857

conditions that delay the closure of aortic valve eg. LBBB, patent ductus arteriosus, severe aortic stenosis

Question 858

Way to remember the type of S2 split that occurs in different conditions?

Answer 858

• normal during inspiration
• Reversed/paradoxical split (left): LBBB
• Widely split (right): RBBB
• Fixed split: ASD
• Loud S2: HTN
• Soft S2: aortic stenosis

Question 859

Innocent murmurs heard in children?

Answer 859

• Ejection murmurs
• Venous hums
• Still/s murmur

Question 860

Innocent murmurs in children: ejection murmurs due to?

Answer 860

Turbulent blood flow at outflow tract of the heart

Question 861

Innocent murmurs in children: venous hums?

Answer 861

due to turbulent blood flow in great veins returning to the heart, heard as a continuous blowing noise just below the clavicles

Question 862

Innocent murmurs in children: Still’s murmur?

Answer 862

low-pitched sound heard at the lower left sternal edge

Question 863

Characteristics of an innocent ejection murmur ?

Answer 863

• soft-blowing murmur in the pulmonary area or short buzzing murmur in the aortic area
• may vary with posture
• localised with no radiation
• no diastolic component
• no thrill
• no added sounds (e.g. clicks)
• asymptomatic child
• no other abnormality

Question 864

Types of murmurs? (6)

Answer 864

• ejection sytolic
• pansystolic (holosystolic)
• late systolic
• early diastolic
• mid-late diastolic
• continuous machine-like murmur

Question 865

Causes ff ejection systolic murmur heard louder on expiration?

Answer 865

aortic stenosis and hypertropic obstructive cardiomyopathy

Question 866

Causes of ejection systolic murmur heard louder on inspiration?

Answer 866

pulmonary stenosis and atrial septal defect

Question 867

Causes of ejection systolic murmurs? (5)

Answer 867

• TOF
• aortic stenosis
• hypertrophic obstructive cardiomyopathy
• pulmonary stenosis
• ASD

Question 868

Causes of holosystolic (pansystolic) murmurs? (3)

Answer 868

• mitral regurg (high pitched and blowing)
• tricuspid regurg (high and blowing)
• VSD (harsh)

Question 869

Why does tricuspid regurg become louder during inspiration, unlike mitral regurg?

Answer 869

during inspiration, venous blood blow to RA and V are increased -> increases stroke volume of RV during systole

Question 870

Causes of late systolic murmur? (2)

Answer 870

mitral valve prolapse and coarctation of aorta

Question 871

Causes of early diastolic murmur?

Answer 871

• aortic regurg
• pulmonary regurg (Graham-Steel murmur)

Question 872

Causes of mid-late diastolic murmur?

Answer 872

• mitral stenosis
• severe aortic regurg (Austin-Flint murmur)

Question 873

Causes of continuous machine-like murmur?

Answer 873

Patent ductus arteriosus

Question 874

What does mitral, tricuspid, aortic and pulmonary regurgitation sound like?

Answer 874

high pitched and blowing

Question 875

What does a pansystolic murmur from VSD sound like?

Answer 875

harsh in character

Question 876

What does mitral stenosis and severe aortic regurg sound like?

Answer 876

rumbling in character

Question 877

What does RILE mean in regards to heart murmurs?

Answer 877

R.ight sided murmur -> heard best on I.nspiration

L.eft sided murmur -> heard best on E.xpiration

Question 878

What does aortic stenosis sound like?

Answer 878

Harsh in character

Question 879

Aortic vs mitral stenosis murmur sound?

Answer 879

Aortic: harsh systolic
Mitral: rumbling diastolic with opening snap

Question 880

What is a leg ulcer?

Answer 880

break in the skin below the knee which has not healed within 2w

Question 881

Venous leg ulcer?

Answer 881

Leg ulcer that occurs in the presence of venous disease (most common type of leg ulcer-60-80%)

Question 882

Where do venous leg ulcers occur typically?

Answer 882

in the gaiter area of the leg (from ankle to mid calf)

Question 883

Causes of leg ulceration?

Answer 883

venous disease; arterial disease; DM; RA; vasculitis; sickle cell; malignancy; drugs

Question 884

What drugs can cause leg ulcers?

Answer 884

NSAIDs, corticosteroids, nicorandil

Question 885

What is venous leg ulceration caused by?

Answer 885

sustained venous HTN resulting from chronic venous insufficiency due to venous valve incompetence or impaired calf muscle pump

Question 886

RFs for venous leg ulcer?

Answer 886

obesity, immobility, increasing age, varicose veins, Hx of DVT

Question 887

Healing and recurrence rates of venous leg ulcers?

Answer 887

Repeat cycles of ulceration, healing and recurrence common.
12m recurrence: 26-69%.
6m healing rates= ommunity 45% and specialist 70%

Question 888

How to examine venous leg ulcer?

Answer 888

• wound= site, edge, size, depth, wound bed, infection
• leg= oedema, varicose veins, venous skin changes, reduced ankle mobility

Question 889

Ix for venous leg ulcers?

Answer 889

• examination
• Doppler assessment of both legs to determine ankle-brachial pressure index in both legs to exclude arterial insufficiency
• consider bloods

Question 890

Primary care Mx of venous leg ulcer?

Answer 890

• cleaning and dressing wound
• compression therapy if appropritate (4 layer compression banding after excluding arterial disease)
• consider pentoxifylline improve healing
• advice
• follow up to assess
• Mx of Cx and associated conditions
• recurrent: refer to vascular specialist ?superficial venous surgery

Question 891

Why may pentoxifylline be prescribed for venous leg ulcers?

Answer 891

to improve microcirculatory blood flow and improve ulcer healing (a peripheral vasodilator)

Question 892

Lifestyle advice to promote leg ulcer healing and reduce recurrence?

Answer 892

compression therapy; keep mobile with walking regular (exercise calf muscle pump function); elevate legs when immobile; emollient frequently

Question 893

When to arrange specialist referral for venous leg ulcer?

Answer 893

Delayed or no healing >2w of adequate Mx or uncertain diagnosis/cause.
For superficial venous surgery.

Question 894

How to reduce risk of recurrence after leg ulcer has healed?

Answer 894

• long-term below-knee graduated compression hosiery
• lifestyle measures
• review and follow up

Question 895

When should bacteriological swabs be taken for leg ulcer?

Answer 895

only if evidence of infection

Question 896

In venous leg ulcers, after ABPI is done, may consider bloods- why?

Answer 896

-FBC: anaemia may delay healing; raised WBC & platelts- infection
- ESR & CRP
- urea and creatinine= high urea- ?dehyrdation which impair healing
- albumin= low may be associated wioth protein loss and malnutrition, may delay healing
- HbA1c: ?DM

Question 897

What is the ankle brachial pressure index (ABPI)?

Answer 897

provides index of vessel competency by measuring ratio of SBP at ankle to that of the arm, valve of 1=normal.

always interpret in context of CP

Question 898

ABPI ratio <0.5

Answer 898

severe arterial disease- compression treatment contraindicated and urgent referral for specialist vascular assessment

Question 899

ABPI ratio >0.5 and <0.8?

Answer 899

arterial disease or mixed arterial/venous disease; refer and generally avoid compression

Question 900

ABPI ratio 0.8-1.3?

Answer 900

no evidence of signif arterial disease and compression safe

Question 901

ABPI >1.3?

Answer 901

may suggest presence of arterial calcification eg. in DM, RA, atherosclerosis, CKD.

may be misleadingly high so refer

Question 902

Features of venous insufficency?

Answer 902

brown pigmentation, oedema, lipodermatosclerosis, eczema

Question 903

Mx for infected leg ulcer?

Answer 903

500mg flucloxacillin 4 times a day for 7 days
or 500mg clarithromycin twice a day

Question 904

Marjolin’s ulcer?

Answer 904

Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb

Question 905

Arterial ulcers?

Answer 905

• Occur on the toes and heel
• Typically have a ‘deep, punched-out’ appearance
• Painful
• There may be areas of gangrene
• Cold with no palpable pulses
• Low ABPI measurements

Question 906

Neuropathic ulcers?

Answer 906

• Commonly over plantar surface of metatarsal head and plantar surface of hallux
• The plantar neuropathic ulcer is the condition that most commonly leads to amputation in diabetic patients
• Due to pressure
• Management includes cushioned shoes to reduce callous formation

Question 907

Pyoderma gangrenosum?

Answer 907

• Associated with inflammatory bowel disease/RA
• Can occur at stoma sites
• Erythematous nodules or pustules which ulcerate

Question 908

Why can’t you use compression for arterial ulcers?

Answer 908

will reduce blood supply further, surgery may be needed to clear out blocked artery (angioplasty)

Question 909

Arrhythmogenic right ventricular cardiomyopathy (ARVC)?

Answer 909

form of inherited CVD that may present with syncope or sudden death; 2nd most common cause of sudden cardiac death in young after hypertrophic cardiomyopathy

Question 910

Pathophysiology of ARVC?

Answer 910

• autosomal dominant
• RV myocardium is replaced by fatty and fibrofatty tissue

Question 911

CP of ARVC?

Answer 911

palpitations, syncope, sudden cardiac death

Question 912

Ix for ARVC?

Answer 912

• ECG= T wave inversion; 50% have epsilon wave (terminal notch in QRS complex)
• echo= subtle; enlarged hypokinetic RV with thin free wall
• MRI can show fibrofatty tissue

Question 913

Mx of ARVC?

Answer 913

• sotalol (antiarrhythmic)
• catheter ablation to prevent V tach
• implantable cardio-verter defib

Question 914

Naxos disease?

Answer 914

autosomal recessive variant of ARVC

triad= ARVC, palmoplantar keratosis and woolly hair

Question 915

Atrial myxoma?

Answer 915

Most common primary cardiac tumour.
Females
75% in LA; commonly attached to fossa ovalis

Question 916

Features of atrial myoxoma?

Answer 916

• systemic= dysponea, fatigue, weight loss, pyrexia of unknown origin, clubbing
• emboli
• AF
• mid-diastolic murmur, ‘tumour plop’
• echo= pedunculated heterogenous mass typically attached to fossa ovalis region of interatrial septum

Question 917

Effects of BNP?

Answer 917

vasodilator
diuretic and natriuretic
suppressess both sympathetic tone and renin-angiotensin-aldosterone system

Question 918

What may cause raised BNP?

Answer 918

produced by LV myocardium in response to strain

HF, MI, LV dysfunction, valvular disease
CKD

Question 919

How to reduce BNP?

Answer 919

ACEinhh
ARB
and diuretics

Question 920

<100pg/ml BNP makes what unlikely?

Answer 920

HF

Question 921

Oxygenation of the blood in the heart?

Answer 921

• deoxygenated blood -> R side of heart via SVC and IVC, oxygen sat 70%; RA, RV, PA have oxyegn sat of around 70%.
• lungs oxygenate blood to around 98-100%; LA, LV and aorta should therefore have oxygen sat 98-100%

Question 922

Oxygen sats you would expect if normal?

Answer 922

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=100%
Aorta= 100%

Question 923

Oxygen sats you would expect if ASD?

Answer 923

RA= 85%
RV= 85%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

Question 924

Oxygen sats you would expect if VSD?

Answer 924

RA= 70%
RV= 85%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

Question 925

Oxygen levels you would expect in PDA?

Answer 925

RA= 70%
RV= 70%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

Question 926

Oxygen levels you would expect in VSD with Eisenmenger’s?

Answer 926

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=85%
Aorta= 85%

Question 927

Oxygen levels you would expect in PDA with Eisenmenger’s?

Answer 927

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=100%
Aorta= 85%

Question 928

Oxygen levels you would expect in ASD with Eisenmenger’s?

Answer 928

RA= 70%
RV= 70%
PA= 70%

LA= 85%
LV=85%
Aorta= 85%

Question 929

What cardiac enzyme/protein marker is used to look for reinfarction?

Answer 929

CK-MB

Question 930

Troponin T and Troponin I?

Answer 930

proteins found in cardiomyocytes; released into blood when heart muscle in damaged eg. MI.

Troponin T= binds the troponin complex to tropomyosin (another protein invl in muscle contraction)

Troponin I= inhibits the interaction between actin and myosin (proteins that cause muscle contraction) when the heart is at rest

Question 931

How is Troponin T and Troponin I used to detect heart muscle damage eg. following MI?

Answer 931

troponins rise in the blood within 3-6hrs after heart muscle damage occurs; peak after 12-24hrs and can remain elevated for up to 1-2w

Question 932

Troponin vs NT-proBNP?

Answer 932

T= diagnose MI; indicates heart muscle damage; highly specific to heart muscle injury

NT-proBNP= diagnose and manage HF (released by heart in response to increased pressure and vol overload eg. in HF); indicates heart strain or overload; reflects HF but can be elevated in other conditions eg. kidney disease, PE, old age

Question 933

BNP vs NT-proBNP?

Answer 933

Both released by ventricles in response to increased pressure and vol overload eg. HF.
BNP is the active hormone and NT-proBNP is the inactive fragment.
NT-proBNP is more stable in the blood and has a longer half-life- 1-2hrs (BNP 20mins) so preferred marker for diagnosing & monitoring of HF.

Question 934

Eisenmenger’s syndrome?

Answer 934

the reversal of a left to right shunt in a congenital heart defect due to pulmonary HTN; occurs when an uncorrected L-to-R shunt leads to copulmonale (pulmonary HTN and obstruction of pulmonary blood due to remodeling of pulmonary microvasculature).

Question 935

What is Eisenmenger’s associated with?

Answer 935

VSD
ASD
PDA

Question 936

Features of Eisenmenger’s?

Answer 936

• original murmur may disappear
• cyanosis
• clubbing
• RV failure
• haemoptysis, embolism

Question 937

Mx of Eisenmenger’s?

Answer 937

heart-lung transplant required

Question 938

Hypothermia?

Answer 938

unintentional reduction of core body temp:
mild= 32-35C
moderate/severe= <32C

Question 939

What happens in the initial stages of hypothermia?

Answer 939

thermoreceptors in skin and subcut tissues sense low temp and cause regional vasocontriction; causes hypothalamus to stimulate release of TSH and ACTH; also stimulates heat production by promoting shivering

Question 940

Causes/RFs of hypothermia?

Answer 940

• elderly and newborn babies
• exposure to cold environment
• inadequate insulation in operating room/general anaesthesia
• hypothyroidism
• impaired mental status
• homelessness
• cardiopulmonary bypass

Question 941

Signs of hypothermia?

Answer 941

• shivering
• cold pale skin
• frostbite
• slurred speech
• Mild= tachypnoea, tachy, HTN
• moderate= resp dep, bradycardia, hypotension
• confusion/impaired mental state

Question 942

Frostbite in hypothermia?

Answer 942

when skin and subcut tissue freeze, causing damage to cells

Question 943

Hypothermia in babies?

Answer 943

can look healthy
may be limp; unusually quiet and refuse to feed.
Extremely common in newborns= hat and blanket soon after birth.

Question 944

Ix for hypothermia?

Answer 944

• temp= tracked over time; low-reading rectal thermometers or thermistor probs
• ECG= acute ST-elevation and J waves or Osborn waes
• FBC + U&Es= Hb elevated, platelets & WBCs low (sequestration in spleen)
• Blood glucose= stress hormones increased so more resistance to insulin
• ABG
• Coag factors
• CXR

Question 945

What should be monitored in hypothermia?

Answer 945

temp
potassium as can be hypokalaemic due to shift of potassium into intracellular space

Question 946

Mx for hypothermia?

Answer 946

• remove from cold & any wet clothing
• warm with blankets
• secure airway and monitor breathing
• not responding to warming then maintain circulation using warm IV fluids or apply forced warm air directly onto body
• RAPID REWARMING can lead to PERIPHERAL VASODILATION AND SHOCK= so if severe prepare for CPR; avoid IV drugs if possible as likely to have drastic response to the drug

Question 947

Advice for pubic on what NOT to do if pt has hypothermia (due to risk of cardiac arrest)?

Answer 947

• don’t put in hot bath
• don’t massage limbs
• don’t use heating lamps
• don’t give alcohol to drink

Question 948

Mx for choking?

Answer 948

1) “are you talking”= if respond yes or able to speak, cough or breath then mild airway obstruction. If unable to speak/they nod, unable to breathe, wheezy, silent cough, unconscious then severe.

2) Mild= encourage pt to cough

2) Severe and conscious=
- 5 back-blows
- unsuccessful then 5 abdo thrusts
- if unsuccessful then repeat

2) if unconscious= call ambulance and start CPR

Question 949

Isolated systolic HTN (ISH)?

Answer 949

Common in elderly; 50% of >70yrs.
Mx in same way as standard HTN.

Question 950

Where is a non-pulsatile JVP seen?

Answer 950

superior vena caval obstruction

Question 951

Kussmaul’s sign: paradoxical rise in JVP during respiration?

Answer 951

seen in constrictive pericarditis

Question 952

JVP: jugular vein waveform= ‘a’ wave?

Answer 952

atrial contaction
- large if atrial pressure eg. tricuspid stenosis, pulmonary stenosis, pulmonary HTN
- absent in AF

Question 953

JVP: jugular vein waveform= cannon ‘a’ waves?

Answer 953

• caused by atrial contractions against a closed tricuspid valve
• seen in complete heart block, V tachy/ectopics, nodal rhythm, single chamber ventricular pacing

Question 954

JVP: jugular vein waveform= ‘c’ wave?

Answer 954

closure of tricuspid valve
- not normally visible

Question 955

JVP: jugular vein waveform= ‘v’ wave?

Answer 955

• due to passive filling of blood into atrium against closed tricuspid
• giant v waves in tricuspid regurg

Question 956

JVP: jugular vein waveform= ‘x’ descent?

Answer 956

fall in atrial pressure during V systole

Question 957

JVP: jugular vein waveform= ‘y’ descent?

Answer 957

opening of tricuspid valve

Question 958

Long saphenous vein?

Answer 958

may be harvested for bypass surgery or removed as Mx for varicose veins with saphenofemoral junction incompetence

Question 959

Path of the long saphenous vein?

Answer 959

• Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the foot
• Passes anterior to the medial malleolus and runs up the medial side of the leg
• At the knee, it runs over the posterior border of the medial epicondyle of the femur bone
• Then passes laterally to lie on the anterior surface of the thigh before entering an opening in the fascia lata called the saphenous opening
• It joins with the femoral vein in the region of the femoral triangle at the saphenofemoral junction

Question 960

Long saphenous vein tributaries?

Answer 960

• Medial marginal
• Superficial epigastric
• Superficial iliac circumflex
• Superficial external pudendal veins

Question 961

Short saphenous vein path?

Answer 961

• Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the foot, which attaches to the great saphenous vein.
• It passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along the posterior aspect of the leg (with the sural nerve)
• Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein, approximately at or above the level of the knee joint.

Question 962

Path of the subclavian artery?

Answer 962

• The left subclavian comes directly off the arch of aorta
• The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into the subclavian and the right common carotid artery.
• From its origin, the subclavian artery travels laterally, passing between anterior and middle scalene muscles, deep to scalenus anterior and anterior to scalenus medius. As the subclavian artery crosses the lateral border of the first rib, it becomes the axillary artery. At this point it is superficial and within the subclavian triangle.

Question 963

Branches of the subclavian artery?

Answer 963

• Vertebral artery
• Internal thoracic artery
• Thyrocervical trunk
• Costocervical trunk
• Dorsal scapular artery

Question 964

Takotsubo cardiomyopathy?

Answer 964

type of non-ischaemic cardiomyopahty associated with a transient, apical ballooning of the myocardium.

may be triggered by stress

Question 965

Pathophysiology of Takotsubo cardiomyopathy?

Answer 965

Takotsubo= Japanese word that for octopus trap

• apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap)

Question 966

Features of Takotsubo cardiomyopathy?

Answer 966

• chest pain
• features of HF
• ECG= ST elevation
• normal coronary angiogram

Question 967

Mx and prognosis of Takotsubo cardiomyopathy?

Answer 967

Mx is supportive.
Prognosis= most improve with supportive treatment.

Question 968

Wolf-Parkinson White?

Answer 968

caused by congenital accessory conducting pathway between A & Vs leading to atrioventricular re-entry tachy (AVRT). As the accessory pathway doesn’t slow conduction, AF can degenerate rapidly to VF.

Question 969

Possible ECG features of Wolf-Parkinson White?

Answer 969

• short PR interval
• wide QRS with slurred upstroke- delta wave
• left axis deviation if right-sided accessory pathway; right axis D if left sided A P (majority have left axis deviation)

Question 970

Differentiate between type A and B of WPW syndrome?

Answer 970

type A (left-sided pathway): dominant R wave in V1

type B (right-sided pathway): no dominant R wave in V1

Question 971

Associations of WPW syndrome?

Answer 971

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

Question 972

Mx of WPW syndrome?

Answer 972

definitive treatment= radiofrequency ablation of the accessory pathway

medical therapy= sotalol***, amiodarone, flecainide

sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation