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Year 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Ischaemic heart disease (IHD) / Coronary artery disease (CAD) / Coronary heart disease (CHD)

A

All interchangeable terms for the condition of inadequate perfusion of the myocardium due to atherosclerosis of the coronary arteries leading to ischaemia & hypo perfusion of myocardial tissue

leading cause of mortality in the UK

incidence ↑ with age

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2
Q

IHD / CAD / CHD risk factors

A 
↑ age
smoking 
hypertension
hyperlipidaemia
diabetes
obesity
elicit drug use
male gender 
inacitivity / sedentary lifestyle
Family history of IHD
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3
Q

Presentations of IHD / CAD / CHD

A

angina pectoris (cardinal symptom)
-retrosternal chest pain / pressure
-may radiate to L arm/neck/jaw
dyspnoea, dizziness, palpitations, nausea & vomiting, sweating

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4
Q

Stable vs unstable angina

A

Stable angina:

  • brought on by exercise
  • symptoms are reproducible
  • symptoms subside with rest or use of GTN

Unstable angine:

  • a type of ACS
  • symptoms start randomly, including at rest
  • not reproducible
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5
Q

Investigations for IHD / CAD / CHD (angina)

A 
resting ECG (often normal)
FBC
Cholesterol
HbA1c
coronary angiogram (Gold standard) 
consider exercise testing
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6
Q

Management of angina pectoris

A

For all patients with IHD:

  • sublingual glyceryl trinitrate (GTN)
  • 75mg aspirin
  • 80mg statin

1st line:

  • beta blockers or calcium channel blockers (CCB)
  • CCB monotherapy use rate limiting agents e.g. diltiazem or verapamil
  • Beta blocker monotherapy use atenolol/bisoprolol/propanolol
  • NB if poor response go to max dose of either drug

2nd line:

  • Beta blocker + CCB
  • use dihydropyridine CCB e.g. MR nifedipine/amlodipine
  • DO NOT combine beta blocker with cerpamil/diltiazem due to risk of severe bradycardia

-less prefers options in combination with either a beta blocker or CCB include long acting nitrates (e.g. isosorbide mononitrate), ivabradine, ranolazine, nicorandil

3rd line:

  • CCB + beta blocker + long acting nitrate/ivabradine/ranolazine
  • only add 3rd drug if pt awaiting revascularisation e.g. with PCI/CABG
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7
Q

What calcium channel blockers should not be combined with beta blockers

A

DO NOT combine beta blocker with verapamil/diltiazem due to risk of severe bradycardia

NB ivabradine should also not be used with verapamil or diltiazem

beta blockers are safe to combine with dihydropyridine CCBs e.g amlodipine/nifedipine/felodipine

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8
Q

1st line angina treatment

A

Beta blockers or calcium channel blockers (CCB)

  • CCB monotherapy use rate limiting agents e.g. diltiazem or verapamil
  • Beta blocker monotherapy use atenolol/bisoprolol/propanolol
  • NB if poor response go to max dose of either drug before adding a further medication
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9
Q

2nd line angina treatment

A

Add a 2nd drug

Preferred 2nd line treatment

  • Beta blocker + CCB
  • use dihydropyridine CCB e.g. MR nifedipine/amlodipine
  • DO NOT combine beta blocker with verpamil/diltiazem due to risk of severe bradycardia

Other 2nd line options
-Beta blocker or CCB + long acting nitrates (e.g. isosorbide mononitrate)/ivabradine/ranolazine/nicorandil

NB ong acting nitrates (e.g. isosorbide mononitrate)/ivabradine/ranolazine/nicorandil can all be used as monotherapy fi both beta blockers & CCB contraindicated or not tolerated

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10
Q

3rd line angina treatment

A

Add a 3rd drug
CCB + beta blocker + long acting nitrate/ivabradine/ranolazine
-only add 3rd drug if pt awaiting revascularisation e.g. with PCI/CABG

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11
Q

Nitrate tolerance

A

pts taking nitrates long term experience reduced efficacy as tolerance develops

asymmetrical dosing should be used to counteract this

pts taking standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance

NB this is not seen with OD MR isosorbide mononitrate

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12
Q

Acute coronary syndrome (ACS)

A

a spectrum of acute myocardial ischaemia and/or infarction

medical emergency requiring immediate hospital admission

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13
Q

Types of Acute coronary syndrome (ACS)

A

Unstable angina:

  • acute myocardial ischaemia not severe enough to caused detectable quantities of myocardial injury
  • troponin not elevated
  • no ST elevation

Non-ST elevation myocardial infarction (NSTEMI)

  • ↑ troponin
  • no ST elevation on ECG
  • ECG may show non specific ST depression, T wave inversion

ST segment elevation MI (STEMI)

  • troponin ↑
  • ST elevation in 2 contiguous leads on ECG
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14
Q

General presentation of Acute coronary syndrome (ACS)

A 
angina at rest/with minimal exertion 
angina not relieved by rest / GTN spray
prolonged angina >20 min 
severe, persistent/worsening angina 
chest pain radiating to L arm, neck, jaw
diaphoresis, syncope, palpitations, nausea, vomiting
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15
Q

Investigations for Acute coronary syndrome (ACS)

A

ECG
troponin
consider echocardiogram
coronary angiogram

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16
Q

Risk assessment on Acute coronary syndrome (ACS)

A

GRACE score

TIMI score

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17
Q

Management of unstable angina

A 
aspirin 300mg 
IV morphine for pain (if required)
IV/sublingual nitrates 
O2 if needed 
offer antithrombin therapy e.g. fondaparinux
offer clopidogrel/ticagrelor

PCI/coronary angiography is reserved for pts who are clinically unstable (immediate) or if GRACE score >3% (within 72h)

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18
Q

Myocardial infarction (MI)

A

ischaemic necrosis of myocardial tissue usually secondary to IHD/CAD/CHD

most commonly affects anterior or inferior territories

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19
Q

Risk factors for Myocardial infarction (MI)

A 
atherosclerosis 
↑ age
male gender
FH of IHD
premature menopause
smoking
diabetes
obesity
HTN
hyperlipidaemia
physical inactivity 
south asian / indian heritage
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20
Q

Presentation of Myocardial infarction (MI)

A

chest pain (often central)

  • radiating to L arm, neck, jaw
  • may present as epigastric pain
  • substernal pressure, squeezing, crushing
diaphoresis
nausea & committing
dyspnoea
fatigue
palpitations 
pt is pale, clammy
altered mental state

atypical presentations are seen in women, elderly and diabetics

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21
Q

Investigations for Myocardial infarction (MI)

A

ECG

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22
Q

Investigations for Myocardial infarction (MI)

A

ECG (ST elevation or ST depression, peaked T-waves, T-wave inversion, Q waves, new onset conduction defects e.g. LBBB)
FBC (leukocytosis common)
U&Es, lipid profiel. CRP
cardiac enzymes e.g. troponin (↑)
CXR
coronary angiogram/myocardial perfusion scan

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23
Q

ECG features of Myocardial infarction (MI)

A 
hyperacute T waves
ST elevation or ST depression
T wave inversion 
Q waves 
new onset LBBB
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24
Q

ECG leads representing septal myocardium

A

Leads V1 & V2

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25
Q

ECG leads representing anterior myocardium

A

Leads V3 & V4

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26
Q

ECG leads for anteroseptal MI

A

V1, V2, V3, V4

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27
Q

ECG leads for lateral MI

A

I, aVl, V5, V6

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28
Q

ECG leads for inferior MI

A

II, III, aVF

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29
Q

ECG leads for posterior MI

A

ST depression in leads V1, V2, V3

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30
Q

ECG leads for posterior MI

A

ST depression in leads V1, V2, V3

also Tall, broad R waves, Upright T waves, Dominant R wave in V2

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31
Q

Vessel affected in anterospetal MI

A

Left anterior descending artery

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32
Q

Vessel affected in inferior MI

A

left circumflex artery

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33
Q

Vessel affected in lateral MI

A

right coronary artery or left circumflex depending on L or R dominance

NB 70% of people are right dominant

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34
Q

Vessel affected in posterior MI

A

Posterior descending artery

In approximately 70% of the population, the right coronary artery (RCA) supplies the posterior descending artery (PDA)

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35
Q

NSTEMI management

A

Initial management

  • ECG (ST depression, T wave inversion)
  • troponin (↑)
  • 300mg aspirin
  • IV/sublingual nitrates
  • O2 & Morphine as needed

calculate GRACE score to asses risk of cardiovascular event

PCI:

  • GRACE score >3% = PCI within 72h
  • PCI immediately if unstable e.g. hypotension
  • NB give
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36
Q

NSTEMI/unstable angina management

A

Initial management

  • ECG (ST depression, T wave inversion)
  • troponin (↑)
  • 300mg aspirin (+fondaparinux if no immediate PCI planned)
  • IV/sublingual nitrates
  • O2 & Morphine as needed

calculate GRACE score to asses risk of cardiovascular event

PCI:

  • GRACE score >3% = PCI within 72h
  • PCI immediately if unstable e.g. hypotension
  • NB give ticagrelor/prasugrel & UFH pre PCI

Conservative management:

  • give fondaparinux with aspirin initially if no PCI planned
  • give ticargelor
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37
Q

STEMI management

A

Initial management

  • ECG (ST elevation, new onset LBBB)
  • troponin (↑)
  • 300mg aspirin (+fondaparinux if no immediate PCI planned)
  • IV/sublingual nitrates
  • prasugrel/clopidogrel/ticagrelor (ticagrelor is preferred)
  • O2 & Morphine as needed
  • UFH/LMWH (pre PCI)

Percutaneous coronary intervention (PCI)

  • gold standard
  • ideally within 12h of symptom onset
  • if pt presents within 12h of symptom onset PCI should happen with 120min of presentation
  • if PCI cannot be offered within 120min of presentation give thrombolysis e.g. alteplase/streptokinase

Longterm management
-CABG, not acute

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38
Q

Antiplatelet therapy post MI

A

dual anti-platelet therapy (aspirin + another drug)

if high risk of bleeding give clopidogrel/prasugrel
if low risk of bleeding give ticagrelor

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39
Q

Secondary prevention post Myocardial infarction (MI)

A

dual anti-platelet therapy:

  • low dose aspiring plus clopidogrel/ticagrelor (ticagrelor is preferred)
  • min 4 weeks duration but given longer

beta blockers:
-initially IV on admission then continued PO

ACE inhibitors/ARBS:

Statins
-80mg as secondary prevention e.g. atorvastatin

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40
Q

GRACE score

A

Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment post MI

composed of:

  • age
  • heart rate, blood pressure
  • cardiac (Killip class) and renal function (serum creatinine)
  • cardiac arrest on presentation
  • ECG findings
  • troponin levels

score >3% is an indication for PCI in NSTEMI & unstable angina

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41
Q

Anti-platelet therapy post Myocardial infarction (MI)

A

dual anti-platelet therapy (aspirin + another drug)

if high risk of bleeding give clopidogrel/prasugrel
if low risk of bleeding give ticagrelor

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42
Q

Driving post Myocardial infarction (MI)

A

Must inform the DVLA

Normal driving license:

  • if treated with PCI can drive after 1 week as long as LVEF >40% & not urgent revascularisation planned
  • if not treated successfully treated with PCI then no driving for 4 weeks

heavy goods/passenger carrying
-must stop driving for minimum 6 weeks, then can have a medical assessment before continuing

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43
Q

Complications of Myocardial infarction (MI)

A
  • Cardiac arrest (usually due to VF)
  • chronic heart failure
  • ventricular septal rupture / free wall rupture
  • Dresslers syndrome (pericarditis 2-10 weeks post MI without infectious cause)
  • Acute mitral regurg (due to ischaemic rupture of papillary muscles, has early-to-mid systolic murmur)
  • LV aneurysm
  • cardiogenic shock
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44
Q

Ventricular septal rupture / free wall rupture

A

presents 7-14 days post MI

septal rupture:

  • new onset harsh pansystolic murmur, shock, pulmonary oedema, angina
  • diagnosed on echo
  • requires surgical closure

free wall rupture:

  • usually 1-2 weeks post MI
  • leads to cardiac tamponade & often death
  • requires urgent percardiocentesis & thoracotomy
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45
Q

LV aneurysm

A

presents with persistent ST elevation and left ventricular failure
Thrombus may form within the aneurysm increasing the risk of stroke

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46
Q

Dresslers syndrome

A

2-10 weeks post MI, thought to be autoimmune reaction, so no infective cause found

characterised by a combination of fever, pleuritic pain, pericardial effusion, pericardial friction rub and a raised ESR (may also have fever)

treated with NSAIDs ± colchicine

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47
Q

Hypertension (HTN)

A

a common condition that is usually asymptomatic & detected on routine examination or after the occurrence of a complication

3rd biggest risk factor for premature death / disability

> 1/4 adults have HTN

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48
Q

Aetiology of Hypertension (HTN)

A

Primary (essential) HTN

  • most common
  • unknown cause

Secondary HTN
-e.g. due to renal disease (most common cause of secondary HTN), pregnancy, primary hyperaldosteronism and other endocrine causes e.g. phaeochromocytoma, medication e.g. steroids/COCP/NSAIDs/Leflunomide

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49
Q

Risk factors for Hypertension (HTN)

A 
obesity 
excessive dietary salt intake
stress
lack of exercise 
alcohol intake
↑ age
Family history
male gender
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50
Q

Defining Hypertension (HTN)

A

Stage 1:
BP in surgery/clinic ≥140/90
ABPM/HBPM 135/85-149/94

Stage 2:
BP in surgery/clinic ≥160/100
ABPM/HBPM ≥150/95

Stage 3:
sBP ≥180 or dBP ≥120

Malignant hypertension:
sBP >200, dBP>130 both with signs of end organ damage

White coat HTN:
clinical BP >20/10 higher than ABPM/HBPM

NB offer HBPM/ABPM to any pt with BP ≥140/90

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51
Q

Investigations for Hypertension (HTN)

A

measure BP in every adult every 5 yrs minimum till age 80 then annually
FBC, U&Es, ruine dipstick, ECG, HbA1c, lipid profile
investigate possible secondary cause if suspected

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52
Q

Management of hypertension

A

Lifestyle interventions

  • ↓salt intake
  • ↓ caffeine intake
  • smoking cessation
  • ↓ weight
  • ↑ exercise

Always treat stage 2 HTN pharmacologically
treat Stage 1 pharmacologically if <80 y/o + endoscopic organ damage / renal disease / established CVD / diabetes / Risk ≥10%

Step 1

  • pt <55 y/o / background of T2DM = ACE-Is e.g. ramipril/ARBs e.g losartan (may use ARB if ACE-I causes dry cough)
  • pt ≥55 y/o / black african / afro-caribbean heritage = CCB e.g. amlodipine

Step 2

  • if taking ACE-I/ARB add CCB or thiazide like diuretic e.g. indapamide
  • if taking CCB add ACE-I/ARB or thiazide like diuretic

Step3

  • add third drug
  • ACE-I/ARB + CCB + thiazide like diuretic

Step 4

  • add 4th drug
  • if K+ ≤4.5 add spironolactone
  • if K+ >4.5 add alpha or beta blocker

Step 5
specialist referral

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53
Q

Conditions for pharmacologically treating Hypertension (HTN)

A

Always treat stage 2 HTN pharmacologically
-i.e. BP in surgery/clinic ≥160/100 or ABPM/HBPM ≥150/95

treat Stage 1 pharmacologically if <80 y/o + endoscopic organ damage / renal disease / established CVD / diabetes / Risk ≥10%
-i.e. BP in surgery/clinic ≥140/90 or ABPM/HBPM 135/85-149/94

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54
Q

Step 1 Hypertension (HTN) management

A

pt <55 y/o / background of T2DM

  • ACE-Is e.g. ramipril or ARBs e.g losartan
  • may use ARB if ACE-I causes dry cough

pt ≥55 y/o / black african / afro-caribbean heritage
-CCB e.g. amlodipine

NB ACE-Is have reduced efficacy in these ethnicities

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55
Q

Step 2 Hypertension (HTN) management

A

if taking ACE-I/ARB add CCB or thiazide like diuretic e.g. indapamide

if taking CCB add ACE-I/ARB or thiazide like diuretic

NB if afro-carribean add ARB rather than ACE-I as these have better effect

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56
Q

Step 3 Hypertension (HTN) management

A

add third drug

ACE-I/ARB + CCB + thiazide like diuretic

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57
Q

Step 4 Hypertension (HTN) management

A

add 4th drug after assessing for orthostatic hypotension & discussing adherence

if K+ ≤4.5 add spironolactone
if K+ >4.5 add alpha or beta blocker

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58
Q

BP targets

A

age >80yrs = 150/90 or HBPM of 145/85

age <80yrs = 140/90 or HBPM 135/85

in T2DM = < 140/90 mmHg

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59
Q

Hypertensive crisis

A

BP ≥180/120

presents with headaches, fits, N&V, visual disturbances and chest pain

management is specialist, BP lowering within 24-48h
usually with IV nitroprusside/labetalol/nifedipine
NB in pregnancy use hydralazine
NB if pheochromocytoma use phentolamine

if not treated quickly leads to end organ damage in retinas & kidneys

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60
Q

Acute Heart failure (HF)

A

life threatening emergency of sudden onset/worsening of HF symptoms

may be de novo i.e. no HF background but ~75% of cases are decompensation of known HF

usually seen in age >65yrs

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61
Q

Acute Heart failure (HF) presentation

A

dyspnoea
SOB
↓ exercise tolerance
peripheral/pulmonary oedema

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62
Q

Acute Heart failure (HF) investigations

A

ECG
echo
CXR
BNP/NT-proBNP

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63
Q

Acute Heart failure (HF) management

A

IV furosemide 20-50mg (or bumetanide)
O2 (sats 94-98%)
vasodilators e.g. nitrates (not routine)
CPAP (if respiratory failure)

if hypotensive/cardiogenic shock give inotropes e.g. dobutamine & pressors e.g.noradrenaline
-if refractory consider LVAD

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64
Q

Heart failure (HF)

A

heart is unable to generate sufficient cardiac output to meet the metabolic demands of the body without increasing diastolic pressure

NB congestive heart failure is a term reserved for pts with breathlessness & abnormal Na+, along with water retention leading to oedema

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65
Q

Types of Heart failure (HF)

A

HF with ↓ ejection fraction (HFrEF) = LVEF <40%

HF with preserved ejection fraction (HFpEF) = LVEF >40%

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66
Q

Epidemiology of Heart failure (HF)

A

average age of diagnosis is 77yrs
incidence ↑ with age

HFpEF tend to be older & female compared to HFrEF pts

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67
Q

Aetiology of Heart failure (HF)

A 
CHD/IHD & HTN (most common causes)
valvular heart disease
post MI
cardiomyopathies
toxins e.g. alcohol, cocain
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68
Q

Presentation of Heart failure (HF)

A

Symptoms:

  • dyspnoea on exertion, fatigue, orthopnoea (breathless lying flat), paroxysmal nocturnal dyspnoea
  • peripheral oedema & pulmonary oedema
  • weight gain (fluid retention)
  • syncope, light headedness
  • nocturnal cough ± pink frothy sputum

O/E

  • displaced apex beat
  • RV heave
  • ↑ JVP
  • narrow pulse pressure
  • pulsus alternans
  • bilateral basal end insinuatory crackles
  • tachypnoea
  • peripheral oedema (ankles & sacrum)
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69
Q

Investigations for Heart failure (HF)

A

Echocardiogram
-dilated LV/RV, ↓LVEF, abnormal diastolic filling pressure

B-type natriuretic peptide (BNP) / N-terminal pro BNP (NT-proBNP)

  • both ↑
  • if BNP >400 μL/ml or NT-proBNP >2000 μL/ml = assess with echo in 2 weeks
  • if BNP 100-400 μL/ml or NT-proBNP 400-2000μL/ml = assess with echo in 6 weeks

CXR
-pleural effusion, Kerley B lines, Bat wing sign, cardiomegaly, upper lobe diversion

FBC, U&Es, LFTs, HbA1c, lipid profile, TFTs, ECG, urinalysis

cardiac MRI
-gold standard for wall motion & ventricular volumes

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70
Q

Staging system for Heart failure (HF)

A

New York Heart Association (NYHA) classification of HF

Class I:
no symptoms on ordinary physical exercise

Class II:
slight limitation of physical activity by mild symptoms
no symptoms at rest

Class III:
moderate limitation of less than ordinary physical activity by moderate symptoms
no symptoms at rest

Class IV:
symptoms present even at rest
↑symptoms with any physical activity

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71
Q

Chest Xray findings for Heart failure (HF)

A 
A - Alveolar oedema (Bat wing sign)
B - Kerley B lines
C - Cardiomegaly
D - dilated upper lobe vessels 
E - (pleural) effusion
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72
Q

Management of Heart failure (HF)

A

Lifestyle:
-smoking cessation, ↓dietary salt (~2-3g/day), alter fluid intake, exercise, ↓alcohol

1st Line:

  • Beta blocker + ACE-I/ARB
  • beta blockers e.g. bisoprolol/carvedilol/nebivolol
  • ACE-Is e.g. ramipril/perindopril/lisinopril
  • ARBs e.g. candersartan/losartan

2nd line:

  • add aldosterone antagonist e.g. epleronone/spironolactone to ACE-I + Beta blocker
  • monitor K+ as both ACE-Is and aldosterone antagonists cause ↑ K+

3rd line: (started by HF specialist)
-add ivabradine/sacubitril with valsartan/digoxin/hyrdalazine with a nitrate

Symptomatic:
furosemide / diuretics for fluid overload

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73
Q

Drugs to avoid in Heart failure (HF)

A 
CCBs e.g. verapamil & diltiazem
TCAs
lithium
NSAIDs
corticosteroids
QT prolonging drugs e.g. erythromycin
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74
Q

1st line management for Heart failure (HF)

A

Beta blocker + ACE-I/ARB

  • beta blockers e.g. bisoprolol/carvedilol/nebivolol
  • ACE-Is e.g. ramipril/perindopril/lisinopril
  • ARBs e.g. candersartan/losartan
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75
Q

2nd line management for Heart failure (HF)

A

add aldosterone antagonist e.g. epleronone/spironolactone to ACE-I + Beta blocker

monitor K+ as both ACE-Is and aldosterone antagonists cause ↑ K+

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76
Q

3rd line management for Heart failure (HF)

A

started by HF specialist

-add ivabradine or sacubitril with valsartan or digoxin or hyrdalazine with a nitrate

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77
Q

Aortic stenosis (AS)

A

usually develops secondary to aortic sclerosis of the tricuspid aortic valve

most common valvular heart disease

most commonly due to calcification & fibrosis

↑ risk if bicuspid aortic valve

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78
Q

Most common valvular heart disease (VHD)

A

Aortic stenosis

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79
Q

Presentation of Aortic stenosis (AS)

A

chest pain / angina, dyspnoea
dizziness, exertional syncope
narrow pulse pressure & slow rising pulse
thrill present
soft/absent S2, possible S4, systolic click

ejection systolic crescendo-decrescendo murmur radiating to the carotids
-loudest in R 2nd intercostal space

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80
Q

Aortic stenosis (AS) murmur

A

ejection systolic murmur

  • crescendo-decrescendo
  • radiating to the carotids
  • best heard in R 2nd intercostal space
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81
Q

Aortic stenosis (AS) pulse

A

slow rising pulse

narrow pulse pressure

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82
Q

Investigations for valvular heart disease (VHD)

A 
Echocardiogram
ECG
CXR
coronary angiogram (needed pre-op, if concomitant CAD can be treated in same operation)
cardiac MRI
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83
Q

Investigations for Aortic stenosis (AS)

A

Echo (↑ aortic pressure gradient)
ECG (LV hypertrophy)
CXR
coronary angiogram (pre-op to determine risk)

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84
Q

Management of Aortic stenosis (AS)

A

asymptomatic pts:

  • observed & monitored
  • consider surgery if valvular gradient >40mmHg & LV dysfunction

symptomatic pt:

  • transcatheter aortic valve implantation (TAVI)
  • balloon vavluloplasty if critical stenosis
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85
Q

Aortic regurgitation (AR)

A

characterised by incomplete closure of the aortic valve leaflets leading to reflux of blood into the LV rapidly leading to LV function deteriorating

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86
Q

Aetiology of Aortic regurgitation (AR)

A 
bicuspid aortic valve
rheumatic fever 
infective endocarditis
Marfans & Ehler Danlos
degenerative aorta valve disease

Rheumatic heart disease is the most common cause world wide
In developed world degenerative disease is most common

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87
Q

Presentation of Aortic regurgitation (AR)

A

sudden severe dyspnoea, pulmonary oedema, HF, fatigue
soft S1
de Mussets sign = head bobbing
quinickes sign = nail bed pulsation
wide pulse pressure, collapsing (waterhammer) pulse
Austin flint murmur (in severe AR, mid-diastolic murmur loudest at apex)

early diastolic murmur

  • best heard in R 2nd intercostal space
  • accentuated by pt leaning forward in expiration
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88
Q

Murmur of Aortic regurgitation (AR)

A

early diastolic murmur

  • best heard in R 2nd intercostal space
  • accentuated by pt leaning forward in expiration
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89
Q

Pulse characteristic in Aortic regurgitation (AR)

A 
wide pulse pressure 
collapsing pulse (water hammer pulse)
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90
Q

Management of Aortic regurgitation (AR)

A

Mild to moderate:
-review yearly & echo every 2 years

severe:
-urgent surgery via TAVI

otherwise TAVI should be offered on a non urgent elective basis

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91
Q

Mitral stenosis (MS)

A

caused by ↑ L atrial & ↑ pulmonary arterial pressures

most commonly due to rheumatic fever

other causes include degenerative calcification, SLE, RA

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92
Q

Presentation of Mitral stenosis (MS)

A

progressive dyspnoea, orthopnea, paroxysmal nocturnal dyspnoea
malar flush*
↑ JVP
signs of right HF (peripheral oedema, ascites, pulsatile hepatomegaly)
loud S1 with opening snap
irregularly irregular pulse (with AF)
RV heave

Low-pitched, rumbling mid diastolic murmur loudest in 5th intercostal space midaxillary line

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93
Q

Murmur of Mitral stenosis (MS)

A

diastolic murmur

  • Low-pitched, rumbling
  • mid-diastolic
  • best heard in 5th intercostal space mid-clavicular line
  • loudest with pt in left hand lateral position, with bell in 5th intercostal space mid-axillary line on expiration
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94
Q

Echo finding for Mitral stenosis (MS)

A

hockeys tick sign shaped mitral deformity

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95
Q

Complications of Mitral stenosis (MS)

A

Atrial fibrillation

  • ↑ risk of thromboembolic event
  • Right HF
  • Pulmonary HTN
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96
Q

Management of Mitral stenosis (MS)

A

percutaneous mitral commissurotomy (PMC) = 1st line
-may require pre-surgical trans-oesophageal echo

surgical valve replacement can be used if pt not a candidate for percutaneous intervention

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97
Q

Mitral regurgitation (MR)

A

2nd most common valvular heart disease after aortic stenosis

causes include degenerative MR (most common), post MI or infective endocarditis

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98
Q

Presentation of Mitral regurgitation (MR)

A

generally tolerated well especially if chronic so is asymptomatic

dyspnoea left HF, pulmonary oedema, palpitations, pulmonary HTN
quiet S1, split S2

pansystolic murmur

  • blowing
  • loudest at apex & radiating into axilla, especially in inspiration
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99
Q

Management of Mitral regurgitation (MR)

A

valve repair is preferred over replacement (especially if degenerative)

papillary muscle rupture post MI requires urgent surgery after haemodynamic stabilisation with inotropes and intra-aortic balloon pump

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100
Q

Murmur of Mitral regurgitation (MR)

A

pansystolic murmur

  • blowing
  • loudest at apex
  • radiating into axilla
  • accentuated in left lateral position with bell over the mid-axillary line in inspiration
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101
Q

Tricuspid regurgitation

A

can be secondary to pulmonary HTN or infective endocarditis (especially in IVDU)

pansystolic murmur heard east in L 4th intercostal space

prominent/giant V waves on JVP with pulsatile hepatomegaly & left parasternal heave

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102
Q

Pulmonary stenosis

A

crescendo-decrescendo ejection systolic murmur heard in L 2nd intercostal space at sternal edge

may radiate to back

widely split S2 may be present

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103
Q

Anticoagulation post valve replacement

A

Biological (bioprosthetic) valves:

  • e.g. porcine or bovine valves
  • give 3 months of warfarin and then lifelong aspirin

Mechanical valves

  • lifelong warfarin anticoagulation
  • Target INR
    • aortic: 3.0
    • mitral: 3.5
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104
Q

Atrial fibrillation (AF)

A

the most common sustained cardiac arrhythmia, its a type of supra ventricular tachyarrythmia characterised by uncontrolled atrial activation

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105
Q

Types of Atrial fibrillation (AF)

A

acute: onset in previous 48h
paroxysmal: spontaneous termination of AF within 7 days
persistent: not self terminating, lasting >7 days

Persistent: cannot be cardioverted

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106
Q

Aetiology of Atrial fibrillation (AF)

A

CHD/IHD
HTN
valvular heart disease
hyperthyroidism

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107
Q

Presentation of Atrial fibrillation (AF)

A

often asymptomatic

palpitations, dyspnoea, chest pain, dizziness, tachycardia

irregularly irregular pulse*

may present with TIA or stroke (due to ↑ thrombotic risk)

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108
Q

Investigations for Atrial fibrillation (AF)

A

ECG
-variable R-R intervals, indiscernible/absent P waves, tachycardia

NB if paroxysmal AF suspected then use 24h ambulatory ECG monitoring

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109
Q

Investigations for Atrial fibrillation (AF)

A

ECG
-variable R-R intervals, indiscernible/absent P waves, tachycardia

TFTs, FBC, U&Es, LFTs, coagulation screen
echocardiogram

NB if paroxysmal AF suspected then use 24h ambulatory ECG monitoring

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110
Q

Management of Atrial fibrillation (AF)

A

1st line rate control unless:

  • AF has a reversible cause e.g. sepsis
  • AF believed to be primarily caused by HF
  • new onset AF (i.e. within <48h)
  • for pts where rhythm control is deemed more suitable based on clinical judgement

Rate Control: (generally 1st line)
1st line
-Beta blockers (except sotalol)
-consider rate limiting CCB e.g. verapamil/diltiazem (avoid in HF)
2nd line
-digoxin (especially if pt has sedentary lifestyle)

Rhythm control: (consider if pt symptomatic despite rate control)

  • DC Cardioversion (if >48h of AF its the preferred method, after 3 weeks of anticoagulation ± TOE)
  • Pharmacological
    • Flecainide (avoid in structural heart disease & IHD)
    • Amiodarone (especially in HF & LV impairment)
    • Beta blockers

Dronedarone is used post successful cardio version to maintain sinus rhythm

Anticoagulation:

  • 1st line is DOACs e.g. apixaban/edoxaban/riveroxaban for all pts with CHA2DS2-VASc score ≥2
  • 2nd line is warfarin
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111
Q

Rate control of Atrial fibrillation (AF)

A

1st line

  • Beta blockers (except sotalol)
  • consider rate limiting CCB e.g. verapamil/diltiazem (avoid in HF)

2nd line
-digoxin (especially if pt has sedentary lifestyle or if co-existing HF)

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112
Q

Rhythm control of Atrial fibrillation (AF)

A

consider if pt symptomatic despite rate control or if new onset AF, or clear underlying cause

DC Cardioversion (if >48h of AF its the preferred method, after 3 weeks of anticoagulation ± TOE)

Pharmacological

  • Flecainide (avoid in structural heart disease & IHD)
  • Amiodarone (especially in HF & LV impairment)
  • Beta blockers

Dronedarone is used post successful cardio version to maintain sinus rhythm

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113
Q

Indications for rhythm control 1st line in Atrial fibrillation (AF)

A
  • AF has a reversible cause e.g. sepsis
  • AF believed to be primarily caused by HF
  • new onset AF (i.e. within <48h)
  • for pts where rhythm control is deemed more suitable based on clinical judgement
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114
Q

Anticoagulation for Atrial fibrillation (AF)

A

Assess stroke risk with CHA2DS2-VASc tool & bleeding risk using the ORBIT score

If CHA2DS2-VASc score ≥2 then anticoagulate

Anticoagulation:
1st line is DOACs e.g. apixaban/edoxaban/riveroxaban
2nd line is warfarin

NB do not withhold anticoagulation simply due to age or risk of falls

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115
Q

Tool to determine stroke risk

A

CHA2DS2-VASc tool

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age ≥ 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
Va Vascular disease (including ischaemic
heart disease and peripheral arterial
disease) 1
S Sex (female) 1

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116
Q

Tool to determine bleeding risk

A

ORBIT score

NB Previously the HAS-BLED scoring system was recommended

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117
Q

CHA2DS2-VASc tool scores

A

Score of 0
=No treatment

Score of 1
=Males: Consider anticoagulation
=Females: No treatment (this is because their score of 1 is only reached due to their gender)

Score ≥2
=Offer anticoagulation

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118
Q

Atrioventricular block (Heart block)

A

characterised by the interrupted or delayed conduction between the atria & ventricles

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119
Q

First degree atrioventricular block

A

PR interval fixed at >0.2 sec/200msc
usually asymptomatic
no treatment needed, low chance of progression
rate of SA node is HR

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120
Q

Second degree atrioventricular block

A

Mobitz Type I (Wenckenbach)

  • progressive lengthening of PR interval until a dropped beat occurs (i.e. normal P wave not followed by QRS complex)
  • low risk of progression

Mobitz Type II

  • PR interval is constant & prolonged with intermittent absent QRS complexes
  • usually follow regular conduction pattern e.g. 3:2 (3 P waves : 2 QRS complexes)
  • high risk of progression to complete heart block
121
Q

Third degree degree atrioventricular block (complete heart block)

A

complete dissociation of P waves & QRS complexes (AV dissociatio)
risk of progression to cardiogenic shock/cardiac arrest is high via ventricular asystole

122
Q

Presentation of Atrioventricular block (Heart block)

A

generally asymptomatic especially if 1st degree of Mobitz Type I

complete heart block may present with:

  • syncope, HF, wide pulse pressure, fatigue, dizziness, dyspnoea
  • Stoke-Adams attacks (sudden LOC lasting a few seconds due to intermittent ventricular asystole)
123
Q

Management of Atrioventricular block (Heart block)

A

all symptomatic pts and pts with Third degree (complete heart block) or Mobitz Type II should be treated

  • atropine can be used to counteract bradyarrythmias
  • transcutaneous pacing
  • Pacemaker implantation* (KEY)
124
Q

Left bundle branch block (LBBB)

A

causes of LBBB include MI, HTN, aortic stenosis, cardiomyopathy, digoxin toxicity

ECG:

  • Deep S waves forming W shape in V1
  • wide notched R waves forming M shape in V5, V6 (also I & aVL)
  • William (W in V1, M in V6)

NB new onset LBBB is always pathological (should usually be treated as ACS)

125
Q

Right bundle branch block (RBBB)

A

can be normal variant especially with ↑ age
other causes include RV hypertrophy, PE, cor pulmonate, ASD, MI

ECG:

  • secondary R waves in leads V1 & V2 forming M shape (or Rabbit ears)
  • deep slurred S waves in V6 & I forming W shape
  • MarroW (M in V1, W in V6)
126
Q

Supraventricular tachycardia (SVT)

A

a group of narrow complex tachyarrythmias arising from abnormalities in pacemaker activity and/or conduction of the atria and/or AV node

generally paroxysmal arrhythmia, i.e. episodes of SVT that self terminate

127
Q

Types of Supraventricular tachycardia (SVT)

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)
-~2/3 cases

Atrioventricular re-entry tachycardia (AVRT)
-due to accessory pathways e.g. in Wolff-Parkinson white syndrome

128
Q

Presentation of Supraventricular tachycardia (SVT)

A

symptoms may be minimal

palpations, syncope, light-headedness, chest pain, dizziness
during attacks tachycardia (140-250bpm)

129
Q

ECG findings in Supraventricular tachycardia (SVT)

A

narrow QRS complexes (<120ms)
rate typically >150bpm
rhythm is regular

consider 24h Holter monitor to catch paroxysmal episodes

NB wide QRS complexes may be seen in aberrant conduction)

130
Q

Management of Supraventricular tachycardia (SVT)

A

1st line:
-vagal manoeuvres e.g. Valsalva (blow into empty syringe) or carotid sinus massage

2nd line:
-IV adenosine if vagal manoeuvres fail (6mg → 12mg if no effect → 18mg if still no effect)

3rd line:
-DC cardioversion

Prevention:
beta blockers & radio frequency ablation

NB adenosine can cause chest pain & impending sense of doom

131
Q

Wolff-Parkinson white syndrome (WPW)

A

AVRT (a type of SVT) due to congenital accessory pathway conducing between atria & ventricles

can degenerate into VF (leading to sudden death)

may present with headaches, palpitations, syncope, light headedness

ECG findings

  • short PR interval
  • wide QRS with slurred upstroke (delta wave)
  • left axis deviation if right sided pathway or vice versa

mangement include radio frequency ablation / surgical ablation (curative)
and acute epsiodes are terminated with vagal manoeuvres & adenosine

132
Q

ECG features in Wolff-Parkinson white syndrome (WPW)

A

short PR interval
wide QRS with slurred upstroke (delta wave)
left axis deviation if right sided pathway or vice versa

133
Q

Atrial flutter

A

a form of SVT characterised by a succession of rapid atrial depolarisation eaves

ECG:

  • saw tooth pattern
  • atrial rate often ~300/min so heart rate is determined by degree of AV block
  • e.g. if 2:1 block then ventricular rate is ~150/min

managed similar to AF but meds are less affected
may be amenable to cardioversion

134
Q

Ventricular tachycardia (VT)

A

broad complex tachyarrhythmia originating from ventricular atopic focuses

potentially life threatening

135
Q

Types of Ventricular tachycardia (VT)

A

monomorphic VT:

  • commonly due to MI
  • QRS complexes all look similar

polymorphic VT:

  • e.g. due to long QT syndrome / QT prolongation, drug toxicity or electrolyte imbalances
  • QRS complexes are dissimilar
  • can lead into Torsades des pointes
136
Q

Presentation of Ventricular tachycardia (VT)

A 
regular tachycardia
palpitations
shock
syncope
hypotension
dyspnoea
dizziness

if sustained i.e. lasting >30sec causes haemodynamic instability

137
Q

ECG features of Ventricular tachycardia (VT)

A

rate >100 bpm (usually 150-200)
regular
QRS complexes (>120ms or >3 small squares)

NB to be considered VT needs to affect >3 consecutive beats

138
Q

Management of Ventricular tachycardia (VT)

A

Pulseless VT
-as per cardiac arrest guidelines, with defibrillation

unstable VT (↓ CO)
-immediate cardioversion (usually low voltage)

stable VT

  • amiodarone 300mg initially then 900mg IV over 24h
  • lidocaine/procainamide
  • if ineffective cardioversion
  • high risk of deterioration into unstable rhythm

Torsades des pointes:
-IV magnesium sulphate

NB ICDs should be considered for all pts to prevent sudden cardiac arrest

139
Q

Ventricular fibrillation (VF)

A

life threatening broad complex tachyarrhythmia characterised by disorganised high-frequency ventricular contractions leading to diminished CO & haemodynamic collapse

most commonly encountered arrhythmia in cardiac arrest

140
Q

ECG features of Ventricular fibrillation (VF)

A

arrhythmic fibrillation baseline usually >300bpm
indiscernable QRS complexes
no atrial P waves

NB ventricular flutter usually has a ventricular rate of 250-300 but can deteriorate into VF

141
Q

Management of Ventricular fibrillation (VF)

A

as per cardiac arrest guidleines

immediate cardioversion via a defibrillator

142
Q

Brugada syndrome

A

a form of inherited cardiovascular disease that presents with sudden death, most commonly seen in asian populations
autosomal dominant mutation in SCN5A gene

ECG

  • convex ST segment elevation >2mm in >1 of V1/V2/V3 followed by negative T wave
  • partial RBBB
  • change of appearance after giving flecainide/ajmaline

Mangement is an ICD

143
Q

Long QT syndrome

A

inherited condition associated with delayed depolarisation of the ventricles, which can deteriorate into torsades des pointes / VT and cause sudden cardiac death

LQT1 & LQT2 are the most common types and are due to defects in slow delayed rectifier K+ channels

144
Q

Normal QT interval

A

430ms in males

450ms in females

145
Q

Causes of a prolonged QT

A 
Long QT syndrome 
Jervell-Lange-Nielsen syndrome (includes deafness)
Romano ward syndrome 
amiodarone
sotalol
TCAs
SSRIs (especially citalopram)
haloperidol
erythromycin 
ondansetron
chloroquine
146
Q

Features of long QT syndrome

A

Long QT on ECG

exertional syncope (especially while swimming) in LQT1
emotional stress syncope in LQT2

sudden cardiac arrest

147
Q

Management of long QT syndrome

A

ICD

beta blockers (not sotalol as it can prolong QT)

avoid QT prolonging drugs & other precipitants e.g. strenuous exercise

148
Q

Reversible causes of cardiac arrest

A

4 H’s and 4 T’s

The H’s

  • hypoxia
  • hypovolaemia
  • hyper/hypokalaemia
  • hypothermia

The T’s

  • thrombosis (coronary or pulmonary)
  • tension pneumothorax
  • tamponade (cardiac)
  • toxins
149
Q

Types of rhythm in cardiac arrests

A

Shockable rhythms:

  • VF
  • pulseless VT

Non shockable rhythms:

  • PEA (pulseless electrical activity)
  • asystole (flat line)
150
Q

Chest compression in cardiac arrest

A

ratio of chest compressions to ventilation is 30:2 in adults

rate of compression is 100-120 bpm regardless of age

NB CPR should continue while the defibrillator is charging

151
Q

Defibrillation rules in cardiac arrest

A

single shock for VF/pulseless VT followed by 2min of CPR, then repeat the shock

NB if witnessed arrest and VF/pulseless VT then 3 stacked shocks may be delivered before commencing CPR

152
Q

Drug delivery in cardiac arrest

A

IV is 1st line

IO (Intraosseous) is 2nd line if IV access not possible

153
Q

Adrenaline use in cardiac arrest

A

1mg of adrenaline (10ml 1:10,000) is generally used

Non shockable rhythm
-give as soon as possible

Shockable rhythm:
-give once CPR has restarted after 3rd shock

Repeat adrenaline every 3-5min while ALS continues

154
Q

Amiodarone in cardiac arrest

A

only used in shockable rhythms
give 300mg after 3rd shock
then give 150mg after the 5th shock

NB lidocaine can be used as an alternative

155
Q

Thrombolytic drugs in cardiac arrest

A

given if PE is suspected cause

must continue CPR for 60-90min post administration to allow agents to work

156
Q

Peri-arrest algorithm for tachyarrhythmias

A

if adverse features e.g. shock/syncope/MI/HF

Step 1:

  • synchronised DC shocks (up to 3)
  • seek expert help

Step 2:

  • 300mg amiodarone IV over 10-20min
  • repeat shock
  • 900mg amiodarone over 24h
157
Q

Peri-arrest in rhythm with broad QRS (>120ms)

A

irregular:
-seek expert help (may be AF + bundle branch block)

regular:

  • if VT/uncertain rhythm = 300mg amiodarone IV over 10-20min then 900mg over 24h
  • if known SVT with bundle branch block = treat as regular narrow complex tachycardia
158
Q

Peri-arrest in rhythm with narrow QRS (<120ms)

A

irregular:

  • probably AF = control rate with diltiazem or beta blockers
  • if in HF consider amiodarone/digoxin
  • consider anticoagulation after assessing thrombotic risk

regular:

  • vagal manœuvres
  • if vagal manoeuvres fail = adenosine 6mg rapid IV bolus
  • if no effect give another 12mg
  • if still no effect give a further 12-18mg
159
Q

Peri-arrest with bradyarrhythmias

A

if adverse features e.g. shock/syncope/MI/HF
-atropine 500 micrograms IV

  • if not successful consider
    • repeat atropine 500 micrograms IV to max 3mg (i.e. 6 doses)
    • transcutaneous pacing
    • isoprenaline 5 micrograms/min IV
    • adrenaline 2-10micrograms/min IV
  • if still no success
    • arrange expert help
    • arrange transcutaneous pacing

If no adverse features but risk of asystole e.g. recent asystole/Mobitz type II/complete heart block with broad QRS/ventricular pace >3sec

  • atropine 500mcg IV (repeat up to 3mg)
  • transcutaneous pacing
160
Q

Shock & circulatory failure

A

a life threatening circulatory disorder leading to tissue hypoxia, a disturbance in microcirculation and end organ damage

161
Q

Types of shock

A 
septic shock
hemorrhagic shock (a type of hypovolaemic shock)
neurogenic shock
cardiogenic shock 
anaphylactic shock
obstructive shock
162
Q

Presentation of the shocked pt

A 
tachycardia 
tachypnoea
hypotension
altered level of consciousness 
agitation / confusion
lethargy 
↓ GCS
oliguria
cold, mottled extremities 
slow cap refill
diaphoretic / clammy

NB if signs of HF e.g. ↑JVP, crackles at lung bases = suggestive of cardiogenic shock

163
Q

General management of shock

A 
ABDCE assessment 
Resuscitation
vascular access 
identify type of shock (ABG, CXR, ECG, USS, etc)
call for help
164
Q

Management of Hypovolaemic shock

A

stop bleeding
blood products if haemorrhage
IV fluids if fluid loss

165
Q

Management of Cardiogenic shock

A

elevate head
resp support if signs of fluid overload
careful use of IV fluids

166
Q

Management of obstructive shock

A

fluids
vasopressors/inotropes
treat underlying cause e.g. PE or cardiac tamponade

167
Q

Management of distributive shock

A

i.e. septic/anaphylactic/neurogenic shock
fluid resuscitation
vasopressors
treat underlying cause

168
Q

Carotid artery stenosis

A

a narrowing of the lumen of the carotid artery most commonly due to atherosclerotic plague formation in the cervical carotid artery

one of the main risk factors for the cerebrovascular events

area of bifurcation of the common carotid arteries is the most common location

169
Q

Presentation of Carotid artery stenosis

A

most pts are asymptomatic

pts may presents with TIAs or strokes i.e. contralateral weakness/sensory disturbances, ipsilateral vision loss, dysphasia, aphasia, speech ataxia

carotid bruit may be audible on auscultation

170
Q

Investigations for Carotid artery stenosis

A

Carotid artery dopple USS

  • helps quantify luminal stenosis
  • moderate = 50-69%
  • severe ≥70%

CT angiogram head/neck/chest
ECG (MI is biggest cause of mortality post carotid endarterectomy)

171
Q

Management of Carotid artery stenosis

A

BP control
Statins
antiplatelets

Surgical (carotid endarterectomy)

  • especially helpful for severe stenosis
  • consider if stenosis ≥50%
  • urgently if pt is symptomatic (within 48h)
172
Q

Renal artery stenosis

A

narrowing of the renal artery lumen considered angiographically significant if >50% reduction in vessel diameter present, mostly secondary to atherosclerosis

accounts for ~90% of renal vascular disease

173
Q

Presentation of Renal artery stenosis

A

hypertension (severe or early onset)
flash pulmonary oedema
abdominal bruit
CKD (due to ischaemic nephropathy)

174
Q

Investigations for Renal artery stenosis

A 
U&Es (↑ creatinine, ↓K+)
aldosterone:renin ratio (<20)
duplex USS (shows stenosis)
CT angiography (but beware of use of contrast if ↓ renal function)
175
Q

Management of Renal artery stenosis

A

angioplasty with stenting (generally 1st line if surgical intervention required)

if stable then medication preferred

  • treat HTN (ACE-Is/ARBs, CCB, beta blockers)
  • statins
  • consider antiplatelets
176
Q

Fibromuscular dysplasia

A

proliferation of the connective tissue & muscle fibres within arteries leading to stenosis generally seen in middle aged females

accounts for ~10% of renal artery stenosis

presents with HTN, flats pulmonary oedema, abdominal bruit, CKD

management of choice is percutaneous tranluminal angioplasty

NB if young female with AKI after staring ACE-I think about fibromuscular dysplasia

177
Q

Acute mesenteric ischaemia

A

essential a stroke of the bowel, most commonly due to an arterial embolism
commonly affects the superior mesenteric artery (SMA)

Most pts will have background of AF
Most pts are >60y/o

178
Q

Presentation of Acute mesenteric ischaemia

A

moderate to severe colicky/constant abdo pain

  • sudden onset
  • poorly localised
  • pain is disproportionate to clinical findings

later signs

  • vomiting & nausea
  • bloody diarrhoea
  • peritonitis
  • shock
179
Q

Investigations for Acute mesenteric ischaemia

A

CT angiogram is gold standard

180
Q

Management of Acute mesenteric ischaemia

A

emergency laparotomy is usually required
the prognosis is for if laparotomy is delayed

NB with treatment mortality is 50-90%

181
Q

Chronic mesenteric ischaemia (intestinal angina)

A

chronic atherosclerotic disease of the vessels supplying the intestines (very uncommon)

presents with colicky/constant abdo pain, history of weight loss, postprandial pain (intestinal angina) and a feat of eating

diagnosed with CT angiogram

treated with open/endovascular revascularisation

182
Q

Ischaemic colitis

A

compromised blood flow to the colon, this is the most common form of intestinal ischaemia
usually affects watershed areas e.g. splenic flexure between SMA & IMA territories

presents with acute abdomen, bloody stools, peritonitis, and septic shock

AXR shows thumb printing (oedematous thickened mucous indents bowel wall)

management is generally supportive especially if not severe, but laparotomy with bowel resection may be necessary

183
Q

Peripheral arterial disease (PAD)

NB also known as peripheral vascular disease

A

includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower extremities arteries most commonly

Risk factors include smoking, HTN, diabetes, hyperlipidaemia, obesity, physical inactivity

NB the most commonly affected vessel is the femoropopliteal artery leading to calf claudication

184
Q

Presentation of intermittent claudication

A

pain/cramping/paraesthesia/burning on exertion
pt usually walks for a predicted distance before symptoms start
symptoms are relived by rest

Leriche syndrome (seen in cortoiliac disease)

  • bilateral hip/buttock/thigh claudication
  • erectile dysfunction
  • absent/diminished femoral pulses
185
Q

Presentation of critical limb ischaemia

A

rest pain lasting >2 weeks
pain worse at night
limb ulceration
gangrene

186
Q

Presentation of acute limb threatening ischaemia

A 
pale
pulseless
painful
paralysed
paraesthetic 
perishing with cold
187
Q

General presentation of Peripheral arterial disease (PAD)

A 
absent/diminshed pulses
dry atrophic, shiny skin
cool peripheries 
loss of hair on legs
brittle nails 
livido reticularis

NB you must check all lower limb pulses

188
Q

Investigations for Peripheral arterial disease (PAD)

A

Ankle brachial pressure index (ABPI)

  • ≤0.90 is diagnostic
  • ≥1 is normal
  • 0.6-0.9 =claudication
  • 0.3-0.6 = rest pain
  • <0.3 = impeding/critical
USS Doppler (shows location of stenosis)
MRI/CT angiogram (shows location of stenosis)
189
Q

Management of Peripheral arterial disease (PAD)

A

smoking cessation*, weight loss, increased exercise
optimise HTN & diabetes management
All pts to start on 80mg statin (i.e. secondary prevention)
clopidogrel for all symptomatic pts
supervised exercise programmes for all pts

Surgery:
endovascular revascularisation (i.e. bypass, angioplasty or stenting)
amputation is last resort

190
Q

Arterial Ulcers

A

ulceration due to impaired blood flow
risk factors include CHD, history of stroke/TIA, diabetes, PAD, obesity, immobility

presents as distal ulcers (often on dorms of foot/toes), with a punched out appearance and well defined borders, base is greyish granulation tissue & there is minimal bleeding on debridement, they are severely painful especially at night

the limb may show signs of chronic ischaemia e.g. hairlessness, pale skin, weak pulses or nail dystrophy

requires specialist referral

191
Q

Differentiating venus & arterial ulcers

A

Ankle brachial pressure index is helpful

severe nocturnal pain points to arterial ulcer
signs of PAD (e.g. hairlessness, pale skin, weak pulses & nail dystrophy) also point to arterial cause

venous ulcers tend to be painless with stasis dermatitis around ulcer, hyperpigmentation and oedema

192
Q

Venous Ulcer

A

chronic defects of the skin that do not spontaneously heal due to chronic venous insufficiency
risk factors include varicose veins, history of DVT/phlebitis, FH of venous disease

ulcers a typically above medial malleolus with a large shallow appearance and irregular borders, often ooze blood when handled but are painless/mildly painful

the limb may have stasis dermatitis around ulcer, hyperpigmentation and peripheral oedema

1st line management are graduated compression bandages, ± debridement and pentoxifylline

193
Q

Neuropathic ulcers

A

often seen in diabetic neuropathy

usually ulcers ulcer calluses or over pressure points on plantar surface of the foot

have punched out appear cane with deep sinuses, tend to be painless, with ↓ sensation in surrounding area

managed by improving diabetic control or treating the underlying neuropathy
close attention should be paid to shoes & socks to reduce pressure points

194
Q

Dry gangrene

A

gangrene secondary to ischaemia with causes including PAD, vasculitis e.g. Raynauds/scleroderma

presents as areas with grey-black discolouration (usually with clear demarcation between viable & gangrenous tissue), coldness & pallor, numbness

THERE IS NO DISCHARGE

management includes restoring blood supply or amputation if not salvageable (NB auto-amputation possible)

195
Q

Wet gangrene

A

dry gangrene with a superinfection (e.g. strep or staph), or secondary to infection causing blockage of blood vessels

presents with oedema, blistering, discharge (may be pus), wet appearance, foul smelling odour, debridement
generally painful and area becomes black

management includes analgesia, broad spectrum Abx (e.g. metronidazole), surgical debridement
amputation if not controlled

196
Q

Gas gangrene

A 
also known as clostridia myonecrosis
a life threatening bacterial infection with gangrene and the following 3 features
  -muscle necrosis
  -sepsis
  -gas production

due to rapid spread of clostridium perfringens from contaminated wound (surgical or traumatic)

presents with excruciating muscle pain (usually no skin changes only pain), massive oedema, cellulitic skin progressing to dark purple, overlying bullae/vesicles, would smelling discharge, surgical emphysema
also septic shock(tachycardia, hypotension, multi-organ failure)

investigated with CT/X-ray/MRI (gas in soft tissue, feathering pattern), blood cultures, ABG, FBC, U&Es, CRO, LFTs

management includes supportive therapy
surgical debridement (radical) ± amputation
IV Abx

197
Q

Necrotising fasciitis

A

Uncommon but life threatening flesh latin disease usually with a polymicrobial cause

NB frequently seen in diabetic pts especially if taking SGLT-2 inhibitors

presents with systemically ill pts with disproportionately severe pain & only minor early skin changes
pain, swelling, erythema
skin necrosis, crepitus, vesicles/bulllae, grey discolouration, septic shock

clinical diagnosis (if strong clinical suspicion requires explorative surgery)

managed with early & aggressive surgical debridement of affected tissue (repeat daily until infection controlled)
IV broad spectrum Abx e.g. vancomycin + clindamycin + meropenem

198
Q

Fournieres gangrene

A

necrotising fasciitis of the perineum/external genitalia that can rapidly spread to the anterior abdominal wall & gluteal muscles

199
Q

Familial hyperlipidaemia

A

autosomal dominant condition resulting in high LDL cholesterol levels

suspect if total cholesterol >7.5 and/or personal/family history of premature CHD (<60y/o)

200
Q

Diagnosis of familial hyperlipidaemia

A

Simon Broome criteria:
-total cholesterol >7.5 mmol/L in adults / 6.7mmol/L in a child & LDL cholesterol >4.9 mmol/L in adults / >4.0 mmol/L in children
+ tendon xanthomata or evidence of these signs in 1st/2nd degree relatives
OR
DNA evidence of LDL receptor mutation

NB must check to fasting LDL levels to confirm diagnosis

201
Q

Management of familial hyperlipidaemia

A

refer to specialist lipid clinic
offer screening for 1st degree relatives
high dose statins e.g. 80mg atorvastatin

202
Q

Secondary causes of hyperlipidaemia

A

hypertriglyceridaemia:

  • T1DM
  • T2DM
  • obestiy
  • alcohol
  • CKD
  • liver disease

hypercholesterolaemia:

  • nephrotic syndrome
  • cholestasis
  • hypothyroidism
203
Q

Presentation of hyperlipidaemia

A 
xanthomas ( nodule lipid deposits in skin/tendons)
xanthelasma (bilateral yellow flat plaques on upper eyelids)
arcus senile (white/grey opaque ring in corneal margin)
204
Q

Management of hyperlipidaemia

A

Primary prevention:

  • 20mg of a statin (atorvastatin generally 1st line)
  • give if QRisk >10% & age >40, or T1DM or CKD with eGFR < 60

Secondary prevention:
-80 mg statin

NB should take a further lipid profile 3 months after starting statins

Lifestyle modifications are vital

205
Q

Pericarditis

A

an inflammation of the pericardium (outer layer of the heart)

acute: <6 weeks
Chronic: ≥ 4months

206
Q

Aetiology of pericarditis

A 
idiopathic
viral infection e.g. cocksackie virus
TB
uraemia (causes fibrous pericarditis)
trauma
post MI (Dresslers syndrome)
hypothyroidism
malignancy
radiation
RA/SLE/Scleroderma
207
Q

Presentation of acute pericarditis

A 
pleuritic chest  pain
  -worse on coughing/swallowing/deep inspiration
  -better sitting/leaning forward
pericardial fiction rub (high pitched scratching on auscultation)
non productive cough
dyspnoea
fever
flu-like symptoms
208
Q

Presentation of chronic pericarditis

A

constrictive (common post TB):

  • dyspnoea, Right HF (↑JVP, ascites, peripheral oedema hepatomegaly)
  • Kussmaul sign (↑JVP on inspiration)
  • pericardial knock
  • pulsus paradoxusus

effusive-constrictive:
-as above + signs of pericardial effusion (↓HS, ↑JVP)

209
Q

Investigations for pericarditis

A

ECG
-saddle shaped ST elevation in all leads, PR depression

echo
-may show pericardial effusion or thickened pericardium

CXR
-pericardial calcification if constrictive

CRP (↑), FBC (↑WCC), troponin (may be ↑)
consider cardiac MRI

210
Q

Management of pericarditis

A

treat underlying cause

if acute:
-1st line = Colchicine + NSAIDs

chronic constrictive:
-pericardioectomy (gold standard)

211
Q

Pericardial effusion vs cardiac tamponade

A

Pericardial effusion:
-collection of fluid in the pericardial space

Cardiac tamponade:
-fluid in the pericardial space leading to ↓CO & circulatory collapse/shock due to compression of the heart

NB every tamponade is an effusion but not vice versa

212
Q

Aetiology of pericardial effusion

A

haemopericaridum:
-trauma, aortic dissection, cardiac wall rupture, cardiac surgery

serous/serosanginous:
-idiopathic, acute pericarditis, malignancy, uraemia, autoimmune disorders, post-radiotherapy, drug induced (e.g. isoniazid/phenytoin)

213
Q

Presentation of pericardial effusion

A

orthopnoea
retrosternal chest pain
hoarseness/nausea/dysphagia/hiccups (compressive symptoms)
Ewart sign (dullness on percussion of L lung base)

214
Q

Presentation of cardiac tamponade

A

Becks triad:

  • hypotension
  • muffled heart sounds
  • distended neck veins

dyspnoea, tachycardia, absent Y waves on JVP, pulsus paradoxus (drop in BP on inspiration)
obstructive shock
cardiac arrest with PEA

215
Q

Investigations for pericardial effusion/cardiac tampoande

A

ECG
-low voltage, electrical alternans (seen mainly in tamponade) i.e. consecutive QRS complexes alter in height)

echocardiogram (gold standard)
-visualises effusion

consider CXR

NB in a cardiac arrest/unstable pt do not delay pericardiocentesis if a tamponade is suspected

216
Q

Management of pericardial effusion

A

treat underlying condition

pericardiocentesis
-can be USS of CT guided

especially traumatic/purulent effusion may require surgical pericardotomy as pericardiocentesis is insufficent

217
Q

Management of cardiac tamponade

A

may need immediate blind pericardiocentesis

if post traumatic (especially penetrating trauma) & in cardiac arrest then emergency thoracotomy is indicated

218
Q

Infective endocarditis (IE)

A

an infection of the endocardial surface of the heart including valvular structures, the chordae tendinae and mural endocardium

most commonly affects mitral valve in normal people
in IVDU pts often causes tricuspid lesions

219
Q

Pathogens causing Infective endocarditis (IE)

A

staph aureus

  • most common overall
  • especially acute IE in IVDU, and those with prosthetic valves/ICDs/Pacemakers

strep viridans

  • previously the most common cause
  • seen after dental procedures/with poor dental hygiene or developing countries

staph epidermis
-colonises indwelling lines so usually seen in pts post prosthetic valve surgery

NB can be culture negative e.g. HACEK or coxiella brunetti

220
Q

Risk factors for Infective endocarditis (IE)

A 
valvular heart disease
valve replacement 
congenital heart disease
previous IE
IVDU
poor dental hygiene
221
Q

Most common sites for Infective endocarditis (IE)

A

most commonly affects mitral valve in normal people

in IVDU pts often causes tricuspid lesions

222
Q

Presentation of Infective endocarditis (IE)

A

Generally:
fevers, chills, tachycardia, malaise, weakness, night sweats, arthralgia, myalgia, pleuritic chest pain

heart murmur (often new) generally regurg i.e. holsystolic 
palpitations, HF
splinter haemorrhages 
Roth spots (round retinal haemorrhages with pale centre)
Oslders nodes (painful nodules on pads of fingers)
Janeway lesions (non tender macules on palms/soles)

emboli to brain / kidney / spleen

223
Q

Criteria for Infective endocarditis (IE)

A 
Modified Duke criteria:
Infective endocarditis diagnosed if
 -pathological criteria positive, or
 -2 major criteria, or
 -1 major and 3 minor criteria, or
 -5 minor criteria

Pathological criteria:
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criteria:
Positive blood cultures
-two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart
-three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis
-positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
-positive molecular assays for specific gene targets

Evidence of endocardial involvement

  • positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
  • new valvular regurgitation

Minor criteria:

  • predisposing heart condition or intravenous drug use
  • microbiological evidence does not meet major criteria
  • fever > 38ºC
  • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  • immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
224
Q

Investigations for Infective endocarditis (IE)

A

Blood cultures:

  • do not delay Abx if pt unwell
  • take 3 sets of cultures from different sites prior to Abx therapy
  • take monitoring cultures to monitor treatment

echo
-valvular or mobile vegetations

CRP/ESR (↑), FBC (↑WCC)

225
Q

Management of Infective endocarditis (IE)

A

Initially empirical Abx:

  • native valve = amoxicillin ± low dose gentamicin
  • penicillin allergy/MRSA/severe sepsis = vancomycin + low dose gentamicin
  • prosthetic valve = rifampicin + vancomycin + low dose gentamicin

Staph endocarditis:

  • native valve = flucloxacillin
  • prosthetic valve = flucloxacillin + rifampicin + gentamicin

Strep endocarditis:
-Benzylpenicillin ± gentamicin

Surgery:

  • for all IE pts affecting prosthetic valves
  • also pts with HF, resistant infections or aortic abscesses
226
Q

Prophylaxis for Infective endocarditis (IE)

A

Abx prophylaxis was previously recommended but this has now stopped

might still be considered in at risk pts e.g. IVDU but very rare

227
Q

Modified duke criteria

A

Infective endocarditis diagnosed if

  • pathological criteria positive, or
  • 2 major criteria, or
  • 1 major and 3 minor criteria, or
  • 5 minor criteria

Pathological criteria:
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criteria:
Positive blood cultures
-two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart
-three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis
-positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
-positive molecular assays for specific gene targets

Evidence of endocardial involvement

  • positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
  • new valvular regurgitation

Minor criteria:

  • predisposing heart condition or intravenous drug use
  • microbiological evidence does not meet major criteria
  • fever > 38ºC
  • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  • immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
228
Q

Rheumatic fever

A

an autoimmune disease that occurs due to an immunological reaction to recent (2-6 weeks ago) strep progenies (Group a Strep) infection e.g. strep throat

most commonly seen in school aged children

229
Q

Presentation of rheumatic fever

A

constitutional symptoms e.g. fever, malaise, fatigue
migratory polyarthritis
CNS: sydenham chorea (often last, 1-8 month post infection)
skin: subcutaneous nodules, erythema marginatum (centrifugal expanding pink/red rash with well defined borders)

Cardiac: (Rheumatic heart disease)

  • percarditis
  • valvular lesions (~65% effect mitral valve, ~25% is aortic valve)
230
Q

Jones diagnostic criteria

A

Used for rheumatic fever
-evidence of recent strep infection + 2 major criteria / 1 major & 2 minor

Evidence of recent strep infection

  • ↑ streptococi antibodies
  • +ve throat swab
  • +ve rapid group A strep antigen test

Major criteria

  • erythema marginatum
  • sydenhams chorea
  • polyarthritis (migratory)
  • carditis & valvulitis
  • subcutaneous nodules

Minor criteria

  • ↑ESR/CRP
  • pyrexia
  • arthralgia
  • ↑ PR interval
231
Q

Most frequently affected valve in Rheumatic heart disease

A

Mitral valve ~65%

  • early on leads to regurg
  • later leads to stenosis

NB ~25% affects aortic valve

232
Q

Diagnostic criteria for Rheumatic fever

A

Jones diagnostic criteria
-evidence of recent strep infection + 2 major criteria / 1 major & 2 minor

Evidence of recent strep infection

  • ↑ streptococi antibodies
  • +ve throat swab
  • +ve rapid group A strep antigen test

Major criteria

  • erythema marginatum
  • sydenhams chorea
  • polyarthritis (migratory)
  • carditis & valvulitis
  • subcutaneous nodules

Minor criteria

  • ↑ESR/CRP
  • pyrexia
  • arthralgia
  • ↑ PR interval
233
Q

Investigations for rheumatic fever

A 
throat swab
anti streptococcal antibodies
group a strep rapid antigen test
ESR/CRP (↑)
CXR
Echo
234
Q

Management of rheumatic fever

A

Abx
-PO penicillin V or benzylpenicillin

NSAIDs

treat complications e.g. HF

235
Q

Myocarditis

A

an inflammation of the myocardium in the absence of predominant acute/chronic ischaemia characteristic of IHD

usually seen in young pts ~40 y/o

though to be the cause of ~10% of sudden deaths in young adults

236
Q

Aetiology of myocarditis

A 
viral (cocksackie B, HIV)
bacteria (diphtheria, clostridium)
lyme disease
chagas disease
autoimmune
drugs e.g. doxorubicin
237
Q

Presentation of myocarditis

A

may be asymptomatic with only ECG abnormalities

fatigue, chest pain, fever, dyspnoea, palpitations, tachycardia
viral prodrome
arrhythmia (sinus tachycardia, heart block, bradyarrhythmias, ventricular extrasystoles)
acute decompensated congestive HF + dilated cardiomyopathy

S3/S4 gallop on auscultation

238
Q

Investigations for myocarditis

A

ECG

  • non specific ST segment & T wave changes
  • ST elevation/depression

CXR
-congestive HF signs (ABCDE)

creatine kinase/CK-MB (↑)
troponin (↑)
BNP (↑)
ESR/CRP (↑)

239
Q

Management of myocarditis

A

supportive management e.g. give inotropes for hypotension

treat underlying cause e.g. Abx if bacterial

NB can cause dilated cardiomyopathy later on

240
Q

Aortic dissection

A

describes a condition where a separation has occured in the aortic wall intimate causing blood flow into a new flash lumen channel composed of inner & outer layers of the tunica intima

MOST common emergency of the aorta

usually seen age 50-70

241
Q

Risk factors for aortic dissection

A 
HTN, smoking, ↑ cholesterol
Trauma (especially deceleration injuries)
connective tissues disease (ehler danlos, marinas)
Turners & Noonas syndromes
syphilis
pregnancy 
cocaine/amphetamine use
bicuspid aortic valve
242
Q

Classification of aortic dissection

A

Standford classification:

  • A: involves ascending aorta
  • B: does not involve ascending aorta

DeBakey classification:

  • I: aorta/ aortic arch & descending aorta
  • II: ascending aorta only
  • III: descending aorta distal to left subclavian

Types I & II are stanford A, while type III is stanford B

243
Q

Presentation of aortic dissection

A

sudden severe tearing/ripping chest pain

  • may radiate to back (intrascapular)
  • pain migrates as dissection progresses

pulse deficit

  • weak/absent carotid/brachial/femoral pulses
  • wide pulse pressure

Hypertension*/hypotension
-variation >20mmHg of sBP between arms

syncope, diaphoresis

244
Q

Investigations for aortic dissection

A

ECG

  • may show MI
  • non specific ST changes
  • normla ECG

CXR
-widened mediastinum

CT/MRI angiogram
USS & dopple

245
Q

Management of aortic dissection

A

resuscitation & ABCDE approach

  • Stanford type A need immediate surgery
  • Stanford type B can be conservatively managed

aggressively manage HTN

  • aim for BP 100-120mmHg
  • IV labetolol used

NB can lead to aortic rupture which presents as hemorrhagic shock

246
Q

Acyanotic congenital heart defects

A

Ventricular septal defect (VSD)
Atrial septal defect (ASD)
Patent ductus arteriosus (PDA)
Coarctation of the aorta

247
Q

Cyanotic congenital heart defects

A

Tetralogy of Fallot (TOF)
transposition of the great arteries
Ebstein anomaly

248
Q

Epidemiology of congenital heart defects

A

VSDs are the most common
-make up ~30% of defects

ASDs are the most common heart defect diagnosed in adults but overall are less common than VSDs

249
Q

Ventricular septal defect (VSD)

A

most common congenital heart defect, often detected on week 20 anomaly scan

causes include Down’s syndrome, Edward’s syndrome, pate syndrome, or intrauterine infections e.g. TORCH/s

presents with failure to thrive, HF (pallor, hepatomegaly, tachycardia, tachypnoea) and a pan systolic murmur ± a systolic thrill

small defects generally close spontaneously so only need monitoring but larger defects usually cause some degree of HF so need to be surgically closed

250
Q

Ventricular septal defect (VSD) murmur

A

pan systolic murmur ± a systolic thrill

251
Q

Atrial septal defect (ASD)

A

most common congenital heart disease diagnosed in adults, more common in females

associated with Down’s and metal alcohol syndrome

presents with ejection systolic murmur & fixed splitting of S2, and embolisms e.g. stroke

often close spontaneously in childhood but if children are symptomatic then surgery is required

252
Q

Atrial septal defect (ASD) murmur

A

ejection systolic murmur & fixed splitting of S2

253
Q

Patent ductus arteriosus (PDA)

A

failure of ductus arteriosus to close, usually associated with prematurity or maternal rubella infection

presents with left subclavicular thrill, heaving apex beat, a continuous machinery murmur and a large volume bounding & collapsing pulse with a wide pulse pressure

management include indomethacin* or ibuprofen (NSAIDs) for neonates which inhibits prostaglandin synthesis and promotes duct closure

254
Q

Patent ductus arteriosus (PDA) murmur

A

continuous machinery murmur

255
Q

Maintaining a Patent ductus arteriosus (PDA)

A

this may be desirable in pts with other congenital heart defects e.g. cyanotic defects such as transposition of the great vessels
duct is kept open until surgical management of other defect

potency can be maintained using prostaglandin E1

256
Q

Patent foramen ovale (PFO)

A

seen in up to 25% of general population

generally asymptotic unless embolus passes into L atrium leading stroke

257
Q

Coarctation of the aorta

A

congenital narrowing of the descending aorta associates with Turner’s syndrome and bicuspid aortic valves

presents with radio femoral delay, differential cyanosis (cyanosis of lower limbs), a mid systolic murmur, notching of the inferior ribs (only seen in adults), difference of BP in upper & lower limbs

management include prostaglandin E1 to maintain patency of ductus arteriosus with surgical correction or balloon angioplasty

258
Q

Coarctation of the aorta murmur

A

mid systolic murmur

  • loudest over back
  • apical click from aortic valve
259
Q

Tetralogy of Fallot (TOF)

A

most common cyanotic heart defect typically presenting age 1-2 months

Features are VSD, right ventricular hypertrophy, right ventricular outflow tract obstruction/pulmonary stenosis and an overriding aorta

presents with cyanosis, ejection systolic murmur, Tet spells (intermittent hypercyanotic, hypoxic episodes associated with physical/psychological stress)

classically a boot shaped heart is seen on CXR

management is usually a 2 part surgical repair

260
Q

Features of Tetralogy of Fallot (TOF)

A

VSD
right ventricular hypertrophy
right ventricular outflow tract obstruction/pulmonary stenosis
overriding aorta

261
Q

Tetralogy of Fallot (TOF) murmur

A

ejection systolic (due to pulmonary valve stenosis)

easy to remember this if you just know the components

262
Q

Transposition of the great arteries (TGA)

also known as transposition of the great vessels

A

due to failure of aorticopulmonary septum to spiral during sepatation, risk is ↑ in children of diabetic mothers

presents with cyanosis, tachypnoea, loud single S2, prominent right ventricular impulse

on CXR see egg-on-string sign

management includes maintaining a patent ductus arteriosus with prostaglandin E1 and surgical correction within the first 2 weeks of life

263
Q

Ebsteins anomaly

A

low insertion of the tricuspid valve resulting in a large atrium and a small ventricle I.e. atrialisation of the right ventricle

commonly associated with in-utero exposure to lithium e.g. in mothers taking lithium

presents with cyanosis, cardiomegaly, HF, respiratory distress, tricuspid regurg (pansystolic murmur), RBBB, widely split S1 & S2

management include prostaglandin E1 to maintain ductus arteriosus and surgical repair

264
Q

Eisenmengers syndrome

A

described reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension, secondary to uncorrected defects causing remodelling of the pulmonary vasculature

associated with VSD, ASD, PDA (long standing)

presents with disappearance of original murmur, cyanosis, clubbing, RV failure, haemoptysis and embolisms

management its a heart-lung transplant

265
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

A

an autosomal dominant disorder characterised by LV hypertrophy, impaired diastolic filling and abnormalities of the mitral valve

most common genetic heart disease & most common cause of sudden cardiac death in the young

266
Q

Inherited cardiomyopathies

A

Hypertrophic obstructive cardiomyopathy (HOCM)
-autosomal dominant

Arrhythmogenic right ventricular cardiomyopathy (ARVC)
-autosomal dominant

267
Q

Presentation of Hypertrophic obstructive cardiomyopathy (HOCM)

A

most pts are asymptomatic

exertional dyspnoea, angina, syncope following exercise
sudden death (usually due to ventricular arrhythmias)
HF
jerky pulses
large ‘a’ waves
double apex beat
ejection systolic murmur

268
Q

Investigations for Hypertrophic obstructive cardiomyopathy (HOCM)

A

ECG
-prminent Q waves, LV hypertrophy, ST/T wave abnormalities

Echo
-mitral regurg, systolic anterior motion, asymmetric hypertrophy

CXR
-cardiomegaly

exercise testing
cardiac MRI
genetic studies & family screening

MOST common area of hypertrophy is anterior ventricular septum

269
Q

Mangement of Hypertrophic obstructive cardiomyopathy (HOCM)

A 
amiodarone
beta blockers/verapamil
ICD (to prevent sudden death)
dual catheter pacemaker 
endocarditis prophylaxis 
anticoagulation if pts in AF

NB avoid nitrates, ACE-Is, inotropes

270
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

autosomal dominant genetic CVD caused by fibro-fatty replacement of right ventricular myocytes

usually presents in adolescence or early adulthood

most common in males

2nd most common cause of sudden cardiac death in <35y/o only second to HCOM

271
Q

Presentation of Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

palpitations, dyspnoea, angina
presyncope/syncope
RV failure (peripheral oedema, hepatomegaly)
sudden cardiac death (may be first presentation)
-often during exercise

272
Q

Investigations for Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

ECG

  • abnormalities in V1/V2/V3 (usually T wave inversion)
  • epsilon waves i.e. terminal notch in QRS complex

Echo

  • often subtle changes initially
  • RV enlargement
  • RV wall motion abnormalities
  • ↓ RV ejection fraction

Cardiac MRI
-fibrofatty tissue in RV wall

273
Q

Management of Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

sotalol (most widely used antiarrhythmic)
amiodarone ± a beat blocker
catheter ablation to prevent VT
ICD (to prevent sudden cardiac death)

274
Q

Dilated cardiomyopathy

A

characterised by ventricular chamber enlargement & contractile dysfunction with normal LV wall thickness

most common for of cardiomyopathy accounting for ~90% of cases, more common in males

275
Q

Aetiology of dilated cardiomyopathy

A 
idiopathic (most common)
myocarditis
IHD
HTN
alcohol use disorder
cocain abuse
276
Q

Presentation of dilated cardiomyopathy

A 
Heart failure 
-dyspnoea, weakness, fatigue, oedema, ↑JVP, pulmonary congestion, cardiomegaly
loud S3/S4
exercise intolerance
mitral/tricuspid regurg 
AF
277
Q

Investigations for dilated cardiomyopathy

A

CXR

  • ballooning heart
  • cardiomegaly
  • pulmonary oedema

Echo

  • atrial/ventricular
  • ↓ Lv ejection fraction
  • wall motion abnormalities

ECG
-non specific ST/T changes

BNP (↑)

278
Q

Management of dilated cardiomyopathy

A

Beta blockers (for all pts)

loop diuretics & thiazide diuretics for fluid overload
ACE-Is/ARBs if ↓ LVEF
spironolactone
nitrates (if diastolic dysfunction)

Heart transplant if medical management fails

279
Q

Restrictive cardiomyopathy

A

a rare type of cardiomyopathy characterised by marked diastolic dysfunction, normal/near normal systolic function & normal ventricular volumes

least common cardiomyopathy, usually seen in elderly people

280
Q

Aetiology of Restrictive cardiomyopathy

A

usually no underlying cause found

post radiation/surgery
Löfflers endocarditis 
amyloidosis
sarcoidosis 
haemochromatosis
281
Q

Presentation of Restrictive cardiomyopathy

A

HF with normal systolic function

  • dyspnoea, fatigue, loud S3, pulmonary oedema
  • features of RV failure dominant e.g. peripheral oedema or hepatomegaly

AF
-seen in ~75% of pts

282
Q

Investigations for Restrictive cardiomyopathy

A

ECG

  • low voltage QRS complexes
  • AF (absent P waves)
  • conductive disorders e.g. RBBB/LBBB

Cardiac MRI
-to differentiate restrictive cardiomyopathy and constrictive pericarditis

endomyocardial biopsy
-with congo red stain

CXR, echo

283
Q

Management of Restrictive cardiomyopathy

A

in children
-usually idiopathic so transplant is treatment of choice

in adults:

  • management of HF
  • amiodarone (if risk of arrhythmias)
  • anti-coagulation if AF
  • ICD
  • heart transplant if medical management fails
284
Q

Takotsubo cardiomyopathy (Broken-heart syndrome)

A

also known as stress induced cardiomyopathy, is a type of non-ischaemic cardiomyopathy associated with transient, reversible LV dysfunction & apical ballooning of the myocardium

can mimic ACS

NB 90% of pts are post menopausal women

285
Q

Takotsubo cardiomyopathy presentation

A 
retrosternal pain with typical features of angina
dyspnoea
syncope
arrhythmias 
signs of HF/cardiogenic shock
286
Q

Takotsubo cardiomyopathy investigations & management

A

ECG
-ST elevation in precordial leads (V1-V3)

Echo

  • apical LV ballooning
  • LV outflow tract obstruction
  • ↓ LVEF
  • global LV dyskinesia involving apex

coronary angiogram (normal)
Cardiac MRI
troponin (↑), BNP (↑), CK-MB (↑)

Mangement is supportive

287
Q

Varicose veins

A

permanently dilated subcutaneous veins of ≥3mm diameter when measured in the standing position

NB the dilation is secondary to incompetent venous valves allowing retrograde blood flow

most commonly affects legs, due to reflux in the saphenous veins

more common in wome

288
Q

Presentation of varicose veins

A

often the cometic presentation of varicose veins will prompt pts to come in

may have machine, throbbing, itching or leg cramps

skin changes:
-varicose eczema, venous stasis, haemosiderrin deposition, lipodermatosclerossi, atrophic blanche

bleeding, superficial thrombophlebitis, venous ulceration, DVT

289
Q

Investigations for varicose veins

A

Trendelenburg test
Perthes manoeuvre
duplex USS

290
Q

Management of varicose veins

A

conservative:

  • for majority of pts
  • leg elevation
  • weight loss
  • regular exercise
  • compression stockings

secondary care

  • endothermal ablation, foam sclerotherapy
  • surgical ligation or stripping
291
Q

Direct oral anticoagulants (DOACs)

A

e.g. Riveroxaban/Apixaban/Edoxaban (direct factor Xa inhibitors) & dabigatran (direct thrombin inhibitor)

indications:

  • prevention of stroke in non-valvular AF
  • treatment of DVT & PE
  • prevention of VTE post hip/knee surgery

side effects include nausea & GI upset

292
Q

Warfarin

A

affects Vit K dependent clotting factors i.e. clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

indications:

  • mechanical heart valves
  • 2nd line for VTE & AF
  • secondary thromboprophylaxis in antiphospholipid syndrome

Monitored via INR (ratio of pts Prothrombin time (PT) and normal PT)

293
Q

Managing ↑ INR

A

Major haemorrhage:

  • stop warfarin
  • give 5mg Vit K IV
  • prothrombin complex concentrate (PCC)

INR >8.0:

  • No haemorrhage
    • stop warfarin
    • PO Vit K
  • minor haemorrhage
    • stop warfarin
    • IV Vit K

INR 5.0-8.0

  • No haemorrhage
    • withhold 1-2 doses & reduce subsequent warfarin dose
  • minor haemorrhage
    • stop warfarin
    • IV Vit K

NB restart warfarin if INR <5.0
NB Vit K can be repeated if INR is still raised after 24h

294
Q

Aspirin

A

block cyclooxyrgenase 1&2 (Cox 1/2) and blocking thromboxane A2 formation

Indications:

  • secindary prevention of CVD (75mg)
  • Acute MI & ischeamic stroke treatment (300mg)
  • post TIA
  • primary thromboprophylaxis in antiphospholipid syndrome

NB not used in children <16y/o due to risk of Reyes syndrome, the only exception being Kawasaki disease

295
Q

P2Y12 receptor antagonists

A

examples include clopidogrel, ticagrelor and prasugrel

work by inhibiting platelet activation via the P2Y12 receptor

Indications:

  • 1st line in secondary prevention post ischaemic stroke/MI/PAD (NB often combined with aspirin for dual antiplatelet therapy)
  • acute MI (with aspirin, give ticagrelor or prasugrel)

NB generally used with aspiring together or as alternative to aspirin if there is an intolerance

296
Q

Heparins

A

e.g. LMWH or UFH
work by activating antithrombin III

Indications:

  • second line for treatment of PE/DVT
  • management of DVT/PE in pregnancy
  • antiphospholipid syndrome un pregnancy
  • VTE prophylaxis
  • ACS pre PCI

side effects include bleeding, thrombocytopenia, osteoporosis, ↑ K+

Heparin induced thrombocytopenia may be seen especially with UFH

NB given S/C

297
Q

Benefits of unfractionated heparin (UFH)

A

useful in pts with renal failure or ↓ renal function
or in situations where high bleeding risk so rapid anticoagulation reversibility is desirable

increased risk of HIT over LMWH

298
Q

Fondaparinux

A

activates antithrombin III

Indications:

  • superficial thrombophlebitis
  • ACS treatment if not a high bleeding risk & no immediate angiography

NB given S/C

Year 3 (6 decks)

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