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3b General care > Cardiology > Flashcards

Cardiology Flashcards

1
Q

List some differentials for chest pain

A

CARDIAC: angina, MI, pericarditis, aortic stenosis, aortic dissection, rupture of AAA, cardiac tamponade, myocarditis

RESP: pulmonary embolism, pneumothorax, pneumonia, asthma attack

MSK: MSK style chest pain, rib fracture, disc prolapse

GI: GORD, acute oesophagitis, peptic ulcer, acute pancreatitis

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2
Q

Define pericarditis

A

inflammation of the pericardium

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3
Q

What are the causes of pericarditis?

A 
viral ** e.g. coxsackie 
trauma 
TB 
uraemia 
MI
systemic diseases e.g. RA, SLE, scleroderma, rheumatic fever
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4
Q

How does pericarditis present?

A

sharp retrosternal chest pain - worse on inspiration, relieved on bending forward, radiates to the back
+ dyspnoea, flu like symptoms, cough

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5
Q

What are the signs of pericarditis O/E?

A

pericardial rub on auscultation (scratchy)

tachycardia, tachypnoea

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6
Q

What are the ECG changes in pericarditis?

A

saddle shape ST elevation
PR depression
Tachycardia

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7
Q

How is pericarditis treated?

A

NSAIDS + colchicine
treat underlying cause

(investigations: ECG, chest x ray, ECHO)

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8
Q

How can constrictive pericarditis develop?

A

if inflammation continues, fibrosis and shrinking of pericardium restricts cardiac filling

can develop R sided heart failure

CXR: pericardial calcification
O/E: raised JVP on inspiration (Kussmauls sign)
auscultate: pericardial knock

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9
Q

Define angina

A

chest pain caused by insufficient blood supply to the heart muscle

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10
Q

How is angina caused?

A

** CORONARY ARTERY DISEASE **

also: valvular disease, hypertrophic obstructive cardiomyopathy and hypertensive heart disease

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11
Q

Describe the clinical features of stable angina

A

central chest tightness/ pain/ crushing - radiates to neck/ shoulder (+ dyspnoea, sweating, nausea)
precipitated by exertion, emotional stress, cold, heavy meals
relieved by rest or GTN spray within 5-10 mins

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12
Q

What are the signs O/E indicating high cholesterol?

A

xanthelasma
fatty deposits in achilles tendon
corneal arcus

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13
Q

What initial investigations would you do for someone with stable angina?

A 
FBC, cholesterol, TFT, U&E, LFTs
ECG 
ECHO
exercise tolerance test 
myocardial perfusion scintigraphy
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14
Q

How is stable angina diagnosed 1st line?

A

CT coronary angiography - IV contrast given

70% narrowing = significant obstruction to the artery -> indicates need for PCI

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15
Q

What are the adverse effects of coronary angiography?

A 
IV contrast allergies
IV contrast precipitates AKI, not good in kidney pts
exposure to radiation
tolerance of scan
trauma
MI
infection and bleeding risk
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16
Q

What is prescribed for relief of angina?

A

sublingual GTN spray (short acting nitrate) - to take for rapid relief of symptoms or before exertion

+ beta blocker or Ca channel blocker

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17
Q

Which secondary prevention lifestyle measures are included for stable angina?

A 
smoking cessation
weight loss
cardioprotective diet 
increase physical activity 
limit alcohol consumption 
educate patient
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18
Q

What is involved in a cardioprotective diet?

A 
reduced refined sugar
<6g salt/day
5 portions fruit and veg/day 
use olive / rapeseed oil for cooking (avoid butter)
2 portions of fish a week 
choose wholegrain carbs
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19
Q

Which medication is prescribed for someone with angina for secondary prevention?

A
  1. anti platelet - 75-100mg aspirin (COX1+2 inhibitor)
  2. statin - atorvastatin
  3. anti hypertensive - ACE-I

+ beta blocker + GTN spray

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20
Q

What does acute coronary syndrome encompass?

A
  1. unstable angina
  2. NSTEMI
  3. STEMI
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21
Q

Define myocardial infarction

A

necrosis of the myocardial tissue after occlusion of a coronary artery and subsequent ischamia

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22
Q

how is ACS caused?

A
  1. atheromatous plaque builds up
  2. plaque ruptures in coronary artery
  3. thrombus formation
  4. partially or completely obstructs the coronary artery supplying the heart
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23
Q

List the risk factors for coronary artery disease?

A 
men 
elderly 
hypertension
smoking
hyperlipidaemia
diabetes mellitus 
obesity
inactivity / lack of exercise 
1st degree relative with CHD
south asian 
systemic diseases e.g. RA, CKD, psychiatric diseases
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24
Q

What are the clinical features suggesting unstable angina?

A

severe crushing chest pain/ tightness that lasts longer than 15 MINUTES and comes on AT REST

+ sweating, dyspnoea, dizziness, nausea

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25
Q

what are the clinical features suggesting myocardial infarction?

A 
central crushing chest pain >15 minutes - radiates to neck and arm
nausea and vomiting
SOB 
dizziness
sweating
palpitations
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26
Q

Who does “silent MI events” commonly happen to?

A
  • elderly diabetics *

20-30% MI present with no/ atypical symptoms

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27
Q

How can a MI be divided?

A
  1. NSTEMI - no ST elevation, caused by partial or intermittent blockage of artery
  2. STEMI- ST elevation, caused by complete and continuing blockage of the coronary artery
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28
Q

What are the possible ECG changes in NSTEMI?

A

ST depression

t wave inversion

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29
Q

Which initial investigations should be done in someone presenting with chest pain?

A

ECG!!!
if NSTEMI -> do a troponin T and I
if STEMI -> give aspirin and immediate PCI, do not wait for troponin

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30
Q

how is troponin used?

A

troponin T and I done in NSTEMI = cardiac biological markers of cardiac muscle death

if levels high after 4 hours of event -> MI
if levels low -> rule out MI

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31
Q

when are troponin levels high?

A 
MI
pericarditis 
arrhythmias
PE
myocarditis
sepsis
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32
Q

How is an acute MI managed?

A
  1. ABCDE and resus , oxygen
  2. dual anti platelet therapy: aspirin + ticagrelor
  3. morphine + anti emetic
  4. monitor with 12 lead ECG
  5. primary percutaneous coronary intervention indicated within 12 hours of onset of symptoms AND if can be given within 120 minutes of time fibrinolysis could have been given
  6. If not, give fibrinolysis
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33
Q

what advice is given after an mI?

A

no driving or sexual activity for 1 month (if PCI can drive after 1 week)
moderate physical activity

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34
Q

what other cardiac enzymes might be raised in ACS?

A

creatinine kinase
LDH
CK - myocardial band
AST (aspartate transaminase)

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35
Q

What secondary preventative advice is given after MI?

A
  1. cardiac rehabilitation
  2. lifestyle risk factors - smoking cessation, weight loss, 150 mins moderate exercise a week, cardioprotective diet, alcohol consumption within normal limits
  3. medical management: aspirin + Ticagrelor + ACE-I + beta blocker + statin
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36
Q

Which risk score predicts risk of heart attack or stroke within next 10 years?

A

Q- RISK

score >10% = significant risk of event = start on statin

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37
Q

Define aortic dissection?

A

tear in the tunica intima in the wall of the aorta leading to separation of the layers and formation a false lumen

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38
Q

List the risk factors for aortic dissection?

A 
hypertension *
trauma *
syndromes: Marfans, Ehlers Danlos, Noonans, Turners 
pregnancy 
cocaine and amphetamines
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39
Q

describe the clinical features of aortic dissection?

A

severe chest pain - radiates through to back, “tearing”
hypertension
aortic regurgitation

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40
Q

How are aortic dissection classified?

A

stanford classification

TYPE A (2/3)- AD in the ascending aorta and aortic arch (proximal to L subclavian)

TYPE B (1/3) - AD in the descending aorta (distal to L subclavian)

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41
Q

What are the complications of Aortic dissection?

A 
aortic regurgitation
unequal arm pulses and bP
stroke
renal failure
cardiac tamponade 
MI
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42
Q

how are type A aortic dissections managed?

A
  1. morphine and oxygen
  2. IV labetalol - BP controlled so systolic 100-120mmHg
  3. surgical intervention
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43
Q

How are type B aortic dissections managed?

A
  1. morphine and oxygen
  2. IV labetalol to control BP systolic 100-120
  3. bed rest and conservative management
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44
Q

How is aortic dissection diagnosed?

A

MRI

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45
Q

What are the possible complications after an MI?

A 
heart failure - acute ro chronic 
post infarction angina 
sudden death from cardiac arrest or VF
cariogenic shock
Dresslers syndrome
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46
Q

What is dresslers syndrome?

A

pericarditis that occurs 2-6 weeks after MI

symptoms: fever, pleuritic chest pain, pericardial effusion, raised ESR

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47
Q

What is an abdominal aortic aneurysm?

A

dilatation of the layers of the aorta to create a large swelling

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48
Q

List the 4 main risk factors for abdominal aortic aneurysm?

A

hypertension
smoking
male
family history

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49
Q

Which connective tissue disorders are associated with AAA and aortic dissection?

A

marfans

Ehlers danlos

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50
Q

When does a AAA become symptomatic?

A

when it RUPTURES!!!

SEVERE back pain + hypotensive shock + pulsatile abdo swelling

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51
Q

What is the screening programme for AAA?

A

ultrasound done for >65 y/o

if no aortic aneurism (<3cm), then rule it out for life
3-4.4cm - small - rescan every 12 months
4.5-5.4 - medium - rescan every 3 months
>5.5cm - large - refer within 2 weeks to vascular surgery for intervention (1 in 1000)

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52
Q

How is AAA diagnosed?

A

ultrasound **

20% rupture into peritoneal cavity (poor prognosis)
80% rupture posteriorly into retroperitoneal cavity

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53
Q

when is intervention indicated in AAA?

A

if >5.5cm or patient symptomatic c

surgical/ endovascular: synthetic graft inserted to replace aneurysmal segment of aorta

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54
Q

what are the 3 types of AAA?

A

TRUE: saccular and fusiform

FALSE

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55
Q

Define heart failure

A

output of heart is inadequate to meet the needs of the body

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56
Q

Describe the pathology behind heart failure with reduced ejection fraction

A

reduction in contractility of the heart so stroke volume is reduced

ejection fraction = the fraction of the blood that is pumped out of the L ventricle into the aorta from the L ventricle

e.g. total volume of blood in L ventricle is 110ml but only 70ml of that is pumped out into aorta = 70/100 = 64% ejection fraction

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57
Q

what is a reduced ejection fraction?

A

<40% ejection fraction = reduced

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58
Q

Describe the NYHA classification for heart failure?

A

NEW YORK HEART ASSOCIATION CLASSIFICATION

1- no symptoms or limitation to daily activities
2- mild symptoms and slight limitation to daily activities
3- marked symptoms and limitations on activities, comfortable at rest
4- severe symptoms and uncomfortable at rest

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59
Q

what are the causes of L sided heart failure?

A

caused by damage to the myocardium so there is impaired contractility and reduced output of the L ventricle

  1. ischaemic heart disease **
  2. hypertension **
  3. valvular disease
  4. cardiomyopathy
  5. arrhythmias
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60
Q

What are the symptoms of L sided heart failure

A 
dyspnoea 
orthopnoea
fatigue 
peripheral oedema 
poor exercise tolerance
cough + pink frothy sputum 
wheeze
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61
Q

What are the signs of L sided heart failure?

A 
bibasal pulmonary crackles
peripheral oedema
displaced apex beat 
muscle wasting
3rd and 4th heart sound
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62
Q

What are the causes of R sided heart failure?

A

R ventricle has to pump against increase resistance in pulmonary vasculature….

  1. progression from L sided heart failure
  2. chronic lung disease e.g. cor pulmonate, PE
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63
Q

What are the signs of R sided heart failure?

A 
raised JVP
pitting oedema
hepatomegaly
splenomegaly 
nausea
ascites
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64
Q

If suspect heart failure, what is the 1st line investigation of choice?

A

BNP (B Natriuretic peptide)

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65
Q

How is BNP levels interrupted for heart failure?

A

if very high -> ECHO and 2 week wait for specialist

if moderately raised -> ECHO and 6 week wait for specialist

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66
Q

When is BNP raised?

A

it is released in response to ventricular stretch

heart failure, LVH, Ischaemia, sepsis, COPD, diabetes, cirrhosis

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67
Q

How do you assess ejection fraction for heart failure?

A

ECHO

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68
Q

what changes would you see on Chest Xray for heart failure?

A 
A- alveolar oedema
B- Kerley B lines
C- cardiomegaly (>50% cardiothoracic ratio)
D- dilated upper lobe vessels
E- pleural effusion
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69
Q

What is included in the 6 monthly review of heart failure?

A
  1. clinical state - medication adherence, side effects, symptoms
  2. screen for depression with PHQ9
  3. review co-morbidities
  4. bloods- U&E, creatinine, eGFR
  5. functional capacity
  6. nutritional status
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70
Q

How is heart failure managed conservatively?

A

education on heart failure
manage lifestyle - smoking cessation, weight loss, restrict alcohol
cardiac rehabilitation programmes
discuss ways to make life easier e.g. benefits, mobility aids, disability parking badge
vaccinations

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71
Q

How is heart failure with reduced ejection fracture managed medically?

A
  1. LOOP DIURETIC e.g. furosemide - relieve congestion symptoms
  2. ACE-I - improve long term survival
  3. BETA BLCOKER - improve long term survival

consider statin, anti platelet

2nd line: + thiazide diuretic
3rd line: + ivabradine / digoxin

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72
Q

What are the risk factors for peripheral vascular disease?

A

smoking **
hypertension
hyperlipidaemia
diabetes

+ CAD risk factors

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73
Q

which classification system is used for PVD?

A

FONTAINE CLASSIFICATION

  1. asymptomatic
  2. intermittent claudication
  3. ischaemic rest pain
  4. critical limb ischaemia
  5. acute limb Ischaemia

(can also use Rutherford classification)

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74
Q

describe the features of intermittent claudication?

A

burning/ cramping pain in back of calf, thigh or buttock (common iliac artery or internal iliac stenosis) on walking
symptoms worse uphill and “claudication distance”
relieved by rest

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75
Q

describe the features of ischaemic rest pain?

A

severe unremitting pain in foot
worse at night and wake up with pain
relieved by hanging foot over side of bed or on a cold floor
ABPI <0.5

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76
Q

Describe the features of critical limb ischaemia?

A

rest pain in foot for >2 weeks
ulceration
gangrene
ABPI <0.3

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77
Q

What examination findings would you see in peripheral vascular disease?

A

prolonged cap refill
trophic changes: pallor, hairloss, cold, skin change
ulcerations , poorly healing wound
absent/ reduced femoral pulse

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78
Q

How is Ankle Brachial Pressure Index calculated?

A

using doppler ultrasound

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79
Q

what score on ABPI indicates PVD?

A 
1= normal
<0.9 = mild PAD
<0.5 = ischaemic rest pain
<0.3= critical limb ischameia
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80
Q

how does acute limb ischaemia present and how is it caused?

A

when acute thrombus or embolus blocks vasculature so no blood supply

6 P’s: pale, perishingly cold, pulseless, painful, paraesthesia, paralysis

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81
Q

How is acute limb ischaemia managed?

A

urgent revascularisation within 4-6 hours + heparin

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82
Q

What are the complications of peripheral vascular disease?

A 
acute limb ischaemia 
infection
poor wound healing
ulcers
amputation
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83
Q

How is peripheral vascular disease managed conservatively / medically?

A

lifestyle measures: smoking cessation **, good control of diabetes, weight loss, manage HTN

anti platelet therapy: clopidogrel
pain relief: paracetamol + opioid

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84
Q

How is PVD managed surgically?

A

revascularisation with angioplasty and stunning / bypass surgery OR amputation

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85
Q

Describe the pathology of aortic regurgitation?

A
  1. aortic valve is between the L ventricle and aorta
  2. the aortic valve closes on diastole and if it doesn’t close the whole way, the aortic valve becomes incompetent
  3. this allows diastolic blood to flow from the aorta back into the L ventricle
  4. causes dilatation of the L ventricle
  5. leads to left ventricular hypertrophy
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86
Q

What are the causes of aortic regurgitation?

A
  1. infective endocarditis
  2. rheumatic fever
  3. bicuspid valve
  4. degeneration
  5. associations : ankylosing spondylitis, aortic dissection, Marfans, Turners, Ehlers Danlose, SLE
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87
Q

What are the symptoms fo aortic regurgitation?

A

cardiovascular collapse

L sided heart failure - SOBOE etc

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88
Q

Name the murmur in aortic regurgitation

A

early decrescendo diastolic murmur

+ Austin flint (soft rumbling low pitched diastolic murmur)

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89
Q

What are the signs of aortic regurgitation?

A

early diastolic murmur + Austin flint murmur
collapsing water hammer pulse
wide pulse pressure (high systolic but low diastolic blood pressure)
De mussets (head bobbing)

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90
Q

How are valve incompetencies diagnosed?

A

ECHO

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91
Q

How is asymptomatic aortic regurgitation treated?

A

watch and wait
review early with 2 yearly ECHO
for HF: ACE-I , diuretics

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92
Q

How is symptomatic aortic regurgitation treated?

A

valve replacement

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93
Q

what is the most common valvular heart disease?

A

aortic stenosis

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94
Q

What are the causes of aortic stenosis?

A

degenerative calcification**
bicuspid valve
rheumatic fever
williams syndrome

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95
Q

What is the triad for aortic stenosis?

A
  1. chest pain
  2. syncope
  3. L sided heart failure - dyspnoea
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96
Q

Describe the aortic stenosis murmur

A

ejection systolic (crescendo decrescendo)
radiates to carotids
best heard sitting forward and at end of expiration

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97
Q

What are the complications of aortic stenosis?

A

heart failure
microangiopathic haemolytic anaemia
predisposes infective endocarditis

98
Q

How is aortic stenosis managed?

A

valve replacement + warfarin (target INR 2.5-3.5)

99
Q

describe the pathology behind mitral stenosis

A

the mitral valve is between the L atrium and L ventricle -> when mitral valve stiff, increases L atrial pressure -> distention of L atrium -> increases pulmonary artery pressure -> R ventricular failure

100
Q

List the causes of mitral stenosis

A

rheumatic fever
infective endocarditis
degenerative calcification
associations: RA, SLE, amyloid

101
Q

How does mitral stenosis present?

A

often asymptomatic

R sided heart failure symptoms

102
Q

Describe the murmur in mitral stenosis?

A

mid late diastolic murmur - heard in L lateral

103
Q

What are the signs O/E of mitral stenosis?

A

malar flush

signs of RHF: raised JVP, splenomegaly, oedema , displaced apex beat

104
Q

what are the complications of mitral stenosis ?

A

AF
pulmonary hypertension
R sided heart failure

105
Q

List the causes of mitral regurgitation?

A

post MI
infective endocraidtis
rheumatic fever
mitral valve prolapse

106
Q

Describe the murmur in mitral regurgitation

A

pan systolic murmur - radiates to axilla

107
Q

describe the pathology behind infective endocarditis?

A
  1. abnormal valve / previously damaged valve
  2. inflammation
  3. destruction and scarring
  4. vegetations grow on valves
  5. valvular regurgitation
  6. vegetations throw off emboli and cause ischaemia elsewhere in the body
108
Q

What are the main causes of infective endocarditis?

A

streptococcus viridan’s *** - dental procedures
staphylococcus aureus ** - IVDU, indwelling catheters
enterococcus faecalis - pelvic surgery
staph epidermidis - IVDU, prosthetic valves

109
Q

List the risk factors for infective endocarditis?

A 
prosthetic valves
IVDU
dental procedures
surgery 
rheumatic heart disease 
previous IE
110
Q

When would you suspect infective endocarditis?

A

fever + new murmur

normally aortic regurgitation (early diastolic murmur) but iVDU more likely for tricuspid regurg (pansystolic murmur)

111
Q

List the signs + symptoms of infective endocarditis?

A

fever + new murmur

Janeway lesions - painless red macule on thenar
Oslers nodes - painful red blisters at end of toes/ fingers
Roth spots - retinal haemorrhages with pale centre
Splenomegaly
splinter haemorrhages
petechiae / purprua

112
Q

what are the complications of infective endocarditis?

A

MI
stroke
glomerulonephritis

113
Q

How is infective endocarditis diagnosed?

A
  1. blood cultures: 3 separate +ve cultures, 12 hours in between, different sites
  2. ECHO
114
Q

How is infective endocarditis treated?

A

amoxicillin + gentamicin

115
Q

what are the primary causes for hypertension?

A

unknown causes but multifactorial RF including:

  • genetic
  • obesity
  • alcohol
  • caffeine
  • high salt diet
  • socioeconomic factors
116
Q

what are the secondary causes for hypertension?

A
  • renal: polycystic kidney disease, renal artery stenosis
  • endocrine: cushings, phaeochromocytoma, acromegaly, thyroid dysfunction,
  • CV: coarction of the aorta (radio-radial delay)
  • pregnancy: pre-eclampsia
  • drugs: contraceptives, anabolic steroids, adrenaline
  • obstructive sleep apnoea
117
Q

What is classed as hypertension?

A

BP >140/90 mmHg

118
Q

What are the features of benign hypertension?

A

slow gradual rise in hypertension over many years

causes gradual changes in vessels -> constriction, reduced size of lumen, more likely to haemorrhage

119
Q

what are the features of malignant hypertension?

A

sudden rapid rise in BP leading to vascular damage of intimal fibrosis thickening and accelerated arteriosclerosis (fibrinoid necrosis)

symptoms: headache, visual disturbance due to papilloedema, retinal haemorrhages

120
Q

What are the complications of hypertension?

A 
CAD- MI, angina
stroke
haemorrhage 
pulmonary oedema
eclampsia 
papilloedema 
retinopathy
AF
121
Q

How is hypertension staged?

A

STAGE 1: BP > 140/90 mmHg

STAGE 2: BP >150/95 or stage 1 + end organ damage/ CVD/ diabetes/ renal pathology/ Q risk >20%

STAGE 3: systolic >180, diastolic >110mmHg

122
Q

How is stage 1 hypertension treated?

A 
LIFESTYLE MODIFICATION
low salt diet 
weight loss
reduce alcohol intake 
stop smoking 
exercise
123
Q

How is stage 2 hypertension and above treated medically?

A

if <55 y/o -> ACE-I e.g. ramipril, lisinopril

if >55 y/o or afro Caribbean -> calcium channel blocker e.g. amlodipine

if ineffective, ACE-I + Ca channel blocker

+ thiazide like diuretic

+ spironolactone

+ alpha or beta blocker

124
Q

What are the differentials for fall/ collapse

A 
cardiovascular causes of syncope- AV heart block, AF, MI
vasovagal
hypoglycaemia
epilepsy/ seizure
postural hypotension 
shock
125
Q

List the differentials for cardiac arrest / sudden death?

A 
MI 
cardiomyopathy 
ventricular arrhythmias 
drug toxicity 
electrolyte abnormalities e..g. hyperkalaemia 
aortic dissection
aortic stenosis
126
Q

which bacteria causes rheumatic fever?

A

group A beta haemolytic streptococci

127
Q

When does rheumatic fever occur?

A

2-4 weeks after post strep infection e.g. pharyngitis, skin infection

128
Q

What is the criteria for rheumatic fever?

A
  1. evidence of recent strep infection
  2. 2 major or 1 major + 2 minor of:
J- joints large arthritis 
O- valvular disease
N- nodules painless, extensor surfaces
E- erythema marginatum (pale red macule)
S- syndenham chorea - upper limb jerking 
P- PR interval prolonged
E- ESR raised
A- arthralgia 
C- CRP raised
E- elevated temp
129
Q

Describe the ECG of rheumatic fever?

A

ST saddle shape elevation

PR interval prolonged

130
Q

How is rheumatic fever managed?

A
  1. bed rest
  2. benzylpenicillin
  3. NSAIDs
131
Q

Define myocarditis

A

inflammation of the myocardium

132
Q

How is myocarditis caused?

A

viruses ** e.g. coxsackie
bacteria - chlamydia
drugs - alcohol, lead poisoning, methyldopa, chloroquine

133
Q

How does myocarditis present?

A

MI + fever (sudden unexplained cardiac death)

134
Q

How is myocarditis diagnosed?

A

endo-myocardial biopsy

FBC, CK, troponin T/I

135
Q

What is cardiac tamponade?

A

collection of fluid/ pus/ gas/ blood in the pericardial space - results in impaired cardiac ventricular filling -> haemodynamic compromise

136
Q

How is cardiac tamponade caused?

A 
pericarditis
malignancy 
dresslers syndrome
infection 
trauma 
connective tissue e.g. SLE, RA
137
Q

What is Becks triad for cardiac tamponade?

A
  1. muffled
  2. JVP
  3. hypotension
138
Q

How does cardiac tamponade present?

A 
oedema
dyspnoea
tachycardia
tachypnoea 
fatigue 
anxiety
139
Q

how is cardiac tamponade diagnosed?

A

echo

140
Q

How is cardiac tamponade managed?

A
  1. oxygen
  2. volume expansion
  3. increase venous return with legs up
  4. inotrope e.g. dobutamine
141
Q

Describe sinus tachycardia

A

focal tachycardia of HR 100-120 bpm, every p wave followed by QRS

142
Q

List some causes of sinus tachycardia?

A 
exercise
stress
anxiety 
hyperthyroidism / thyrotoxicosis 
sepsis
caffeine 
alcohol
143
Q

Describe atrial flutter

A

type of supraventricular tachycardia where there is a succession of rapid atrial depolarisation

144
Q

Describe atrial flutter ECG

A

SAWTOOTH BASELINE - not every p wave followed by QRS

145
Q

What are the possible causes of atrial flutter?

A 
CAD
HTN
hyperthyroid 
COPD
alcohol
146
Q

How is atrial flutter treated?

A

same as AF

147
Q

Describe supraventricular tachycardia on ECG

A

** narrow complex regular tachycardia **

absence of p waves, narrow QRS, >100 bpm

148
Q

What are the symptoms of SVT?

A

angina type symptoms - chest pain, faintness, SOB

149
Q

How is SVT managed acutely?

A
  1. vagal manoeuvres - carotid sinus massage
  2. IV adenosine
  3. electrical cardio version
150
Q

What is Wolff Parkinson white syndrome?

A

= atrioventricular re-entry tachycardia (AVRT), type of SVT

caused by an accessory conduction pathway called the bundle of Kent -> the additional pathway causes arrhthymias through pre-excitation and re-entry circuits that conduct faster than the AVN

151
Q

Describe the features on ECG of Wolff Parkinson’s white syndrome

A
  1. short PR interval
  2. wide QRS
  3. delta wave (upsloping to QRS - indicates abherant pathway)

L/R axis deviation depending on R/L accessory pathway

152
Q

How is Wolff Parkinson white syndrome treated?

A

radio frequency ablation of the accessory circuit (medication of amiodarone if refuse)

153
Q

Describe ventricular tachycardia on ECG

A

** broad complex regular tachycardia **

no p waves, broad QRS, tachycardia, regular

154
Q

How is VT assessed and subsequently treated?

A

pulse present -> amiodarone, lidocaine

pulse absent -> need to synchronise with DC shock or cardioversion

155
Q

Describe ventricular fibrillation on ECG

A

** broad complex irregular tachycardia”

no p waves, no identifiable QRS or T wave, chaotic, rate 150-500 bpm

156
Q

How does VF present?

A

cardiac arrest!!! LOC, death as no effective output

157
Q

How is VF treated?

A

defibrillation

158
Q

What is torsades de pointes?

A

type of “polymorphic” ventricular tachycardia

159
Q

describe the ECG of torsades de pointes?

A

prolonged QT, prominent U waves

160
Q

How is torsades de pointes caused?

A

drugs - anti arrhthymics, TCA, erythromycin, clarithromycin
hypokalaemia
hypomagnesaemia
IHD

161
Q

How is torsades de pointes treated?

A

IV magnesium sulphate

162
Q

Describe the ECG change in Brugada syndrome?

A

elevated J point , ST elevation

at risk of sudden death (AD inherited condition)

163
Q

How is brugada syndrome treated?

A

ICD implantable cardioverter defibrillator

164
Q

What is an atrioventricular heart block?

A

prolonged PR interval suggesting there is atrioventricular delay -> impaired conduction between the atria and ventricle

165
Q

what are the possible causes of AV heart block?

A

MI/ ischaemia
myocarditis
infection e.g. Lyme disease, infective endocarditis
SLE

166
Q

Describe first degree heart block ECG

A

fixed prolonged PR interval (>200ms/5 little squares)

167
Q

How is first degree heart block treated?

A

asymptomatic and requires no treatment

168
Q

Describe second degree heart block mobitz type 1?

A

PR interval slowly increases until there is a dropped QRS complex

169
Q

How is 2nd degree heart bloc mobitz type 1 managed?

A

asymptomatic and no treatment

170
Q

Describe second degree heart block mobitz type 2?

A

fixed PR interval but sudden dropped beats

171
Q

How is 2nd degree heart block mobitz type 2 treated?

A

dangerous as at risk of sudden cardiac death

need pacing if symptomatic

172
Q

describe 3rd degree heart block?

A

when there is complete heart block - no association between p and QRS waves

173
Q

How does 3rd degree heart block present?

A

syncope
heart failure
regular bradycardia
wide pulse pressure

174
Q

Describe what atrial fibrillation is?

A

irregularly irregular narrow QRS complex with absent p waves

due to atrial myocytes depolarising in uncoordinated fashion

175
Q

What are the causes of AF?

A
  1. elderly , idiopathic **
  2. congestive heart failure **
  3. hypertension **
cardiomyopathy 
CAD
mitral stenosis
alcohol, caffeine 
thyrotoxicosis 
sepsis
176
Q

How does AF present?

A 
asymptomatic
palpitations, chest pain
SOB 
syncope
dizziness
fatigue
177
Q

What is the worrying complication with AF?

A

stasis of blood from ineffective atrial contraction predisposes patient to a thrombus within the L atrium which can throw off emboli causing ischaemic STROKE or ischaemia in other organs

178
Q

Describe the ECG findings on AF?

A

irregular QRS

absent P waves

179
Q

Which further investigations might you do if find AF on ECG?

A 
FBC (anaemia?)
 TFTs** (thyrotoxicosis)
UandE (potassium?)
ECHO (assess for heart failure or valvular abnormalities)
CXR
d- dimer, troponin (ACS?)
180
Q

which score is used to assess stroke risk in AF patients?

A 
CHADS2VASC
C- congestive heart failure
H- hypertension
A- age >75 (2)
D- diabetes
S2- previous stroke or TIA (2)
V-  vascular problems e.g. MI
A- age 65-74
SC - sex category (female = 1)
181
Q

How are CHADS2VASC scores interrupted ?

A 
<2 = low risk -> consider anticoagulant 
>2 = high risk -> start on anti coagulant
182
Q

How is AF managed?

A 
RATE CONTROL: 
beta blocker (atenolol)  OR
cardio selective calcium channel blocker (verapamil) OR
digoxin (better in elderly, sedentary)
 Aim for ventricular rate 60-80bpm

RHYTHM CONTROL:
cardioversion medical: amiodarone
electrical: DC cardio version (if acute)

LONG TERM: warfarin or apixiban

183
Q

How should AF patients be managed conservatively?

A

reduce caffeine and alcohol intake
control BP
treat thyroid disease
inform DVLA is symptoms affect driving

184
Q

when is electrical cardioversion indicated?

A

if a patient unstable

  1. 120-150 J cardioversion
  2. 3x attempts
  3. IV 300mg amiodarone via central line
185
Q

Describe the pathology behind bundle branch blocks

A
  1. conduction blocked in one of the bundle branches of the interventricular septum
  2. the affected area of the myocardium will be stimulated later by conduction from unaffected areas of the myocardium
  3. leads to widening of the QRS
186
Q

What are the possible causes of RBBB?

A 
physiological normal variant 
rheumatic heart disease
IHD
myocarditis 
cardiomyopathy
187
Q

Describe the ECG changes in RBBB?

A

M wave in V1 (second R wave)

W wave in V6 (deeper S wave)

188
Q

What are the causes of LBBB?

A

coronary artery disease ** - more extensive disease
hypertensive heart disease
dilated cardiomyopathy

189
Q

Describe the ECG changes in LBBB?

A

W wave in V1 (deep S wave)

M wave in V6 (broad notched R wave)

190
Q

List the reversible causes of bradycardia and cardiac arrests

A 
H - hypoxia
H - hypothermia
H - hypovolaemia
H - hypokalaemia
T - thrombus 
T - toxin
T- tension pneumothorax
T - tamponade
191
Q

How is bradycardia assessed?

A
  1. ABCDE
  2. obtain IV access, give oxygen
  3. monitor ECG, BP, SpO2, 12 LEAD ECG
  4. identify and treat reversible causes
  5. adverse features present ? shock, syncope, MI, HF?
192
Q

How is bradycardia treated?

A

atropine 500mcg IV

193
Q

What is the mechanism of atropine?

A

blocks vagus nerve to increase the sinus rate and increase AV conduction

194
Q

What are the side effects of atropine?

A 
blurred vision
dilated pupils 
dry mouth
urinary retention
confusion
195
Q

What is sick sinus syndrome?

A

dysfunction of SA node with impairment of ability to generate a pulse causing bradycardia

196
Q

What are the causes of sick sinus syndrome?

A

idiopathic fibrosis of node
ischaemia
digoxin toxicity

197
Q

How is symptomatic sick sinus syndrome treated?

A

dual chamber pacemaker

198
Q

Describe the mechanism of amiodarone?

A

blocks Na/K/Ca channels and an alpha beta adrenergic antagonist
lengthens duration of action potential to slow conduction

199
Q

what are the side effects of amiodarone?

A

hypotension, AV block, grey skin colour

pneumonitis , hepatitis

200
Q

Describe the mechanism of adenosine?

A

blocks conduction through AV node so slows sinus rate and slows conduction

201
Q

How is adenosine given?

A 
short duration (half life of 10s)
IV 6mg
202
Q

what are the side effects of adenosine?

A

bradycardia

systole

203
Q

What are the side effects of Ca channel blockers?

A 
ankle swelling
flushing 
headache
bradycardia
constipation
204
Q

What are the side effects of beta blockers?

A

fatigue
cold extremities
headache
impotence

205
Q

what is digoxin used for?

A

reduce ventricular rate in AF
severe heart failure (3rd line)

= reduces conduction at the AVN

206
Q

Describe the symptoms of digoxin toxicity?

A 
arrthymias
nausea and vomiting 
diarrhoea
dyspnoea
confusion
dizziness
207
Q

What are the 3 types of cardiomyopathy?

A
  1. dilated = most common
  2. hypertrophy
  3. restrictive
208
Q

How is cardiomyopathy diagnosed?

A

ECHO

209
Q

What are the risk factors for dilated cardiomyopathy?

A

alcohol **
familial/ idiopathic **

+ ischaemia, chemotherapy, post partum, hypertension

210
Q

how does dilated cardiomyopathy present?

A

usually asymptomatic until sudden death

211
Q

How is hypertrophy cardiomyopathy caused?

A

familial AD

212
Q

how is restrictive cardiomyopathy caused?

A

elderly

amyloidosis

213
Q

what are the types of AF?

A
  1. paroxysmal - spontaneous termination of AF within 7 d
  2. persistent - lasts more than 7d, not self limiting
  3. permanent - longstanding AF over a year
214
Q

Which score can be used to assess bleeding risk in a patient?

A 
HASBLED
Hypertension
Abnormal liver, renal function
Stroke
Bleeding history
Labile INR
Elderly
Drugs
215
Q

what do scores on HASBLED indicate?

A 
0-2 = consider anticoagulant 
3-5 = alternative to anti coagulants should be used
>5 = high risk of bleeding
216
Q

what are the benefits of DOACs?

A

do not need INR monitoring
faster onset
faster offset
set doses

217
Q

What are the disadvantages of DOACs (direct oral anti coagulants)?

A

limited antidotes

218
Q

what should you tell a patient taking warfarin?

A 
do not miss doses
take at same time every day 
do not get pregnant 
do not eat food high in Vitamin K e.g. broccoli, kale, spinach 
limit alcohol
219
Q

List the differentials for palpitations?

A 
atrial fibrillation 
atrial flutter 
VT 
WPW
AVNRT 
ectopics
220
Q

How are any tachyarrhythmias investigated?

A
  1. ECG
  2. ECHO
  3. stress testing for exercise related
221
Q

How is HF patient treated in an emergency?

A
  1. ABCDE
  2. furosemide IV
  3. monitor renal function - AKI, monitor K, ABG if hypoxic
  4. daily weights
  5. fluid restrict <1.5L/day
  6. catheter
  7. repeat CXR
  8. refer to cardiology
222
Q

What is the mechanism of furosemide (loop diuretic)?

A

competitively inhibits the Na-K- 2Cl co transporter in the thick ascending limb in the loop of Henle

223
Q

Outline the mechanism of aspirin?

A

irreversibly inhibits COX enzyme causing reduced production of prostaglandins and thromboxane A2 - this stops platelet aggregation and prevents further cardiac events

224
Q

outline the mechanism of Ticagrelor

A

P2Y12 receptor antagonist preventing platelet activation and aggregation

SE: dizziness, dyspnoea, hypotension, headache, haemorrhage

225
Q

what is a capture beat?

A

occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.

226
Q

what are shockable rhythms?

A

VF

pulseless VT

227
Q

when do you give adrenaline in an arrest?

A

adrenaline 1 in 10,000 (100mcg/mL)

IV injection repeated every 3-5 minutes

228
Q

What are the signs of pulmonary oedema?

A 
tachycardia
tachypnoea
raised JVP
widespread fine crackles
dull percussion at bases
gallop rhythm
229
Q

How is pulmonary oedema managed?

A
  1. furosemide
  2. oxygen
  3. morphine
  4. GTN/ nitrates
230
Q

describe the ECG changes after MI?

A

pathological Q wave

T wave inversion

231
Q

why should metformin be stopped before angiogram?

A

metformin interacts with IV contrast and precipitates lactic acidosis

232
Q

what are the indications for amputation?

A 
gangrene
trauma
necrosis 
acute limb ischaemia
necrotising fasciitis
233
Q

what are the considerations for an amputation?

A

large enough joint for prosthetic limb?
adequate blood supply to heal stump?
retain as many working joints as possible?

234
Q

what is phantom limb pain?

A

pain experienced below an amputation

= due to hypersensitivity of divided nerves

235
Q

How can phantom limb pain be managed?

A

neuropathic analgesia e.g. gabapentin, pregabalin, amitriptyline

236
Q

what are the complications of an amputation?

A

infection
stump ischaemia
failure to mobilise
pressure sore

237
Q

what are the stages of wound healing?

A

haemostasis
inflammation
proliferation
remodelling

238
Q

how do varicose veins form?

A

incompetent valves in veins allowing vein dilatation and tortuous

239
Q

what are the risk factors for varicose veins?

A

obesity
pregnancy
prolonged standing
conditions: eczema, venous ulceration, oedema

240
Q

what are the possible long term complications of varicose veins?

A

pain
ulceration
psychological effects

3b General care (4 decks)

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