Cardiology Flashcards

1
Q

what is the ratio of chest compressions to ventilation in adults?

A

30:2

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2
Q

what is adrenaline given in a VT/VT cardiac arrest?

A

once chest compressions have restarted after the third shock an then every 3-5 mins (during alternate cycles of CPR)

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3
Q

what are the 2 shockable rhythms?

A

pulseless VT

VF

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4
Q

what happens if a cardiac arrest happens in a cardiac monitored patient?

A

do up to 3 quick successive ‘stackd’ shocks, rather than 1 shock followed by CPR

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5
Q

what is done in asystole/pulseless electrical activity?

A

adrenaline 1mg asap

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6
Q

following successful resuscitation, what oxygen sats should be given?

A

94-98%

to address potential harm caused by hyperoxaemia

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7
Q

what are reversible causes of cardiac arrest?

A

4T’s and 4H’s

Thrombosis
Tension pneumothorax
Tamponade
Toxins

Hypoxia
Hypovolaemia
Hyperkalaemia, hypoglycaemia, hypocalcaemia
Hypothermia

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8
Q

adrenaline dose in a cardiac arrest?

A

cardiac arrest: 10ml 1:10,000 IV or 1ml of 1:1000 IV

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9
Q

adrenaline dose in anaphylaxis?

A

anaphylaxis: 0.5ml 1:1,000 IM

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10
Q

how does adrenaline work?

A

responsible for the fight or flight response
released by the adrenal glands
acts on α 1 and 2, β 1 and 2 receptors
acts on β 2 receptors in skeletal muscle vessels-causing vasodilation

increases cardiac output and total peripheral resistance
causes vasoconstriction in the skin and kidneys causing a narrow pulse pressure

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11
Q

actions of adrenaline on adrenergic receptors?

A

inhibits insulin, stimulates glucagon secretion

lots more actions to raise blood glucose

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12
Q

what is brugada syndrome?

A

inherited cardiovascular disorder which may present with sudden cardiac death
AD inheritance

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13
Q

ECG changes in brugada syndrome?

A

convex ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave

partial right bundle branch block

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14
Q

Ix of brugada syndrome?

A

ECG changes more apparent following administration of flecainide or ajmaline

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15
Q

mx of brugada syndrome?

A

implantable cardioverter-defibrillator

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16
Q

what is syncope?

A

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

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17
Q

features of syncope?

A

trigger- emotion, pain, exercise
prodrome- feeling faint, dizzy, nausea, visual disturbance
pallor
near immediate complete recovery

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18
Q

types of syncope?

A
reflex syncope (neural mediated)
orthostatic syncope
cardiac syncope
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19
Q

causes of reflex syncope

A

vasovagal - emotion, pain, stress
situational- micturition, sneeze etc
carotid hypersensitivity- e.g. shaving, tight collar

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20
Q

causes of orthostatic syncope?

A

insufficient of baroreceptors causes autonomic dysfunction

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21
Q

types of orthostatic syncope?

A

primary autonomic failure- PD, lewy body dementia

secondary autonomic failure- diabetic retinopathy, amyloidosis, uraemia

drug-induced- diuretics, alcohol, vasodilators

volume depletion- haemorrhage, diarrhoea

exercise-induced

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22
Q

causes of cardiac syncope?

A

arrhythmias e.g. sick sinus syndrome, SVT, VT

structural- valvular, MI, hypertrophic obstructive cardiomyopathy

others e.g. PE

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23
Q

questions to ask in a syncope history (5Cs and 5Ps)

A

5Ps- precipitant, prodrome, palpitations, post-event phenomena

5Cs- colour, convulsions, continence, cardiac problems, family history of cardiac death

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24
Q

Ix of syncope?

A
CV examination
postural BP
(fall in SBP by >20 or DBP by >10 is considered diagnostic)
ECG/2hr ECG
Carotid sinus massage
Tilt table test
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25
Q

mx of syncope?

A

if CV cause -> refer (24 hours)
if epilepsy suspected -> refer (2 weeks)
if uncomplicated- arrange ECG within 3 days and reassure and advice of avoiding triggers
if affecting QOL -> offer referral for tilt table test to assess whether syncope is accompanied by a severe cardioinhibitory response

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26
Q

name some genetic causes of primary cardiomyopathy?

A

1) hypertrophic obstructive cardiomyopathy- leading cause of death in young athletes
- usually due to a mutation in the gene encoding B-myosin heavy chain protein

2) Arrhythmogenic right ventricular dysplasia- RV myocardium is replaced by fatty and fibrofatty tissue. 50% have mutation encoding for components of desmosome.
ECG abnormalities- V1-V3, typically T wave inversion, epsilon wave (terminal notch in QRS complex)

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27
Q

mx of Arrhythmogenic right ventricular dysplasia?

A

sotalol, catheter ablation, ICD

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28
Q

name some acquired causes of primary cardiomyopathy?

A
  • peripartum cardiomyopathy- typically develops between last month of pregnancy and 5 months post-partum. More common in older women, greater parity and multiple gestations
  • takotsubo cardiomyopathy- ‘stress’ induced cardiomyopathy i.e. family member has just died. Transient, apical ballooning of the myocardium
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29
Q

name some mixed causes of primary cardiomyopathy?

A
  • dilated cardiomyopathy- alcohol, coxsackie B virus, doxorubicin, post partum hypertension
  • restrictive cardiomyopathy- amyloidosis, post-radiotherapy, Loeffler’s endocarditis
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30
Q

causes of secondary cardiomyopathy?

A
  • infective
  • infiltrative- amyloidosis
  • storage- haemochromatosis
  • toxicity- doxorubicin, alcoholic cardiomyopathy
  • inflammatory sarcoidosis
  • endocrine- DM, thyrotoxicosis, acromegaly
  • neuromuscular- Friendreich’s ataxia, DMD, myotonic dystrophy
  • nutritional deficiency- thiamine
  • autoimmune- SLE
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31
Q

signs and symptoms of dilated cardiomyopathy?

A

acute pulmonary oedema
systemic or pulmonary emboli
congestive cardiac failure (exertional dyspnoea, orthopnoea, PND, fatigue, RUQ pain)

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32
Q

Ix of dilated cardiomyopathy?

A

ECHO
ECG- sinus tachycardia, AF
CXR- heart failure signs

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33
Q

tx of dilated cardiomyopathy?

A
diuretics
ACEi
BB
aldosterone antagonists
antiarrhythmic agents
anticoagulation
cardiac resynchronisation therapy, ICDs
cardiac transplantation
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34
Q

what is the most common cause of cardiac death in the young?

A

hypertrophic obstructive cardiomyopathy

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35
Q

what is hypertrophic obstructive cardiomyopathy?

A

AD disorder of muscle tissue caused by defects in the genes encoding contractile proteins-> most commonly B-myosin heavy chain protein or myosin binding C protein

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36
Q

features of hypertrophic obstructive cardiomyopathy?

A

often asymptomatic
exertional dyspnoea, angina, syncope
arrhythmias, HF, sudden death
jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur increases with Valsalva manoeuvre and decreases on squatting

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37
Q

associations with hypertrophic obstructive cardiomyopathy

A

Friedreich’s ataxia

Wolff-Parkinson white

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38
Q

ECHO findings of hypertrophic obstructive cardiomyopathy?

A

mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

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39
Q

ECG findings of hypertrophic obstructive cardiomyopathy?

A

LVH
non- specific ST segment and T-wave abnormalities, progressive T-wave inversion may be seen
Deep Q waves
AF

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40
Q

mx of hypertrophic obstructive cardiomyopathy?

A
Amiodarone
Beta blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis
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41
Q

what is Friedreich’s ataxia?

A

AR
GAA repeat in X25 gene on chromosome 9
onset age 10-15 years

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42
Q

features of Friedreich’s ataxia?

A

gait ataxia, kyphoscoliosis, absent ankle jerks/extensor plantars, cerebellar ataxia, optic atrophy, spinocerebellar tract degeneration

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43
Q

differentials of chest pain?

A
ACS
pneumothorax
PE
pericarditis
dissection aortic aneurysm
GORD
MSK pain
shingles
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44
Q

features of MI?

A

sudden onset, central crushing chest pain
may radiate into neck and down left arm
signs of autonomic dysfunction- sweating, nausea, pale

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45
Q

what is an NSTEMI?

A

partial thickness necrosis of the myocardium
ST changes- ST depression, T-wave inversion or no changes
no troponin rise

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46
Q

ECG features of previous MI?

A

pathological Q waves

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47
Q

what is a STEMI?

A

full thickness necrosis of myocardium
hyper acute T waves are often first sign
ST elevation- >0.2mV in men and >0.15mV in women in leads V2-V3 and/or >0.1 in other leads

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48
Q

name some cardiac enzymes?

A
Troponin T- rises at 4-6 hours, peaks at 12-24, normal at 7-10 days
CK-MB- returns to normal after 2-3 days
CK
AST
LDH
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49
Q

false positives of troponin T?

A

-itis e.g pericarditis, myocarditis
trauma to heart
CKD
sepsis

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50
Q

medical mx of MI?

A

Morphine- 2.5-10mg IV PRN
O2 (if sats <94%)
GTN- 2 puffs
Aspirin 300mg

perform an ECG but don’t delay transfer to hospital

dual antiplatelet therapy- aspirin and clopidogrel/ticagrelor

unfractionated heparin if going to have PCI

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51
Q

when to refer for chest pain?

A

onset <12 hours with abnormal ECG-> emergency admission
onset 12-72 hours ago-> refer for same day assessment
onset >72 hours ago -> perform ECG and troponin before deciding on action

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52
Q

surgical intervention for MI?

A

PCI within 120 mins (if onset <12 hours ago)

thrombolysis if PCI can’t be done within 120 mins (and onset <12 hours ago)

CABG

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53
Q

types of thrombolysis?

A

tissue plasminogen activator, tenecteplase, alteplase

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54
Q

what needs to be done after thrombolysis?

A

ECG within 90 mins to seen if there has been a >50% resolution in the ST elevation
(if there has not been adequate resolution then rescue PCI)

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55
Q

risks of thrombolysis?

A

reocclusion
intracranial haemorrhage
infection
bleeding

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56
Q

how to thrombolytics work?

A

plasminogen to form plasmin, which degrades fibrin and so breaks up the thrombi

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57
Q

what class of drug is clopidogrel and ticagrelor?

A

P2Y12-receptor antagonist

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58
Q

CI to thrombolysis?

A
active internal bleeding
recent haemorrhage, surgery or trauma
coagulation and bleeding disorders
intracranial neoplasm
stroke <3 months
aortic dissection
recent head injury
pregnancy
severe hypertension
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59
Q

secondary prevention of MI?

A
DAPT- aspirin plus ticagrelor, clopidogrel, prasugrel
ACEi
Beta-blocker
Statins
aldosterone antagonist if MI plus HF

lifestyle- diet, exercise, sex after 4 weeks of uncomplicated MI

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60
Q

complications of MI?

A
cardiac arrest
cardiogenic shock
chronic HF
arrhythmias
pericarditis
aneurysms
left ventricular wall rupture
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61
Q

what are the primary and secondary prevention doses of statins?

A

primary- 20mg

secondary- 80mg

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62
Q

how does aspirin work?

A

antiplatelet
inhibits COX which in turn inhibits production of thromboxane A2

reduces platelets ability to aggregate

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63
Q

what is the GRACE score?

A

a risk stratification tool used for an NSTEMI to decide upon further management
high risk= coronary angiography during admission
low risk= coronary angiography at a later date

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64
Q

what is the pathophysiology of ACS?

A

Atherosclerosis in coronary arteries -> gradual narrowing and reduced O2 reaching myocardium -> plaque rupture causes occlusion and ischaemia of myocardium

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65
Q

unmodifiable risk factors for IHD?

A

increasing age
male
FH

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66
Q

modifiable risk factors for IHD?

A
smoking
DM
Hypertension
hypercholesterolaemia
obesity
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67
Q

ECG changes and coronary territories?

A

anterior- V1-V4 (LAD)
inferior- II,III,aVF (right coronary)
lateral- I, V5-6 (left circumflex)

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68
Q

features of typical angina?

A

1) constricting discomfort in the front of the chest, or in the neck, shoulders, jaw and arm
2) precipitated by physical exertion
3) relieved by rest or GTN in about 5 minutes

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69
Q

features of atypical and non-anginal pain?

A

2 features- atypical

0/1 feature- non-anginal chest pain

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70
Q

mx of stable angina?

A

Attacks- GTN spray

1st line -beta blocker or CCB
if using CCB on its own- use rate-limiting e.g. verapamil or diltiazem

if using BB and CCB, use long-acting dihydropyridine e.g. nifedipine

If still symptomatic on BB and CCB-> only add third drug whilst waiting for PCI or CABG

if can’t tolerate CCB and BB- add long-acting nitrate e.g ivabradine, nicorandil or ranolazine

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71
Q

SE of CCBs?

A

headache
flushing
ankle oedema

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72
Q

SEs of BBs?

A

bronchospasm
fatigue
cold peripheries
sleep disturbances

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73
Q

SEs of nitrates?

A

headache
postural hypotension
tachycardia

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74
Q

SEs of nicorandil?

A

headache
flushing
anal ulceration

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75
Q

what is nicorandil?

A

potassium channel activator

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76
Q

causes of acute pericarditis?

A
viral infections- coxsackie virus, EBV, influenza, HIV
TB
uraemia
trauma
post MI
connective tissue disease
hypothyroidism
malignancy
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77
Q

features of acute pericarditis?

A
pleuritic chest pain relieved by sitting forwards
non-productive cough
dyspnoea
flu-like symptoms
pericardial rub
tachypnoea
tachycardia
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78
Q

ECG changes of acute pericarditis?

A

saddle-shaped ST elevation

PR depression

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79
Q

mx of acute pericarditis?

A

treat underlying cause

NSAIDs and colchicine 1st line for patients with acute idiopathic or viral pericarditis

80
Q

features of chronic pericarditis?

A

dyspnoea
RHF- elevated JVP, ascites, oedema, hepatomegaly
pericardial knock- loud S3
Kussmaul’s sign

81
Q

what is kussmaul’s sign?

A

rise in JVP on inspiration

82
Q

what is heart failure?

A

a reduced cardiac output that results from a functional or structural abnormality

83
Q

common causes of acute heart failure?

A

ACS
hypertensive crisis
arrhythmias
vascular disease

84
Q

symptoms of HF?

A

breathlessness, reduced exercise tolerance, oedema, fatigue

85
Q

important questions in history?

A
  • how many pillows do you sleep with at night?
  • how far can you walk before getting breathless and has this changed from normal?
  • do you have a cough and bring anything up? (pink frothy sputum= pulmonary oedema)
86
Q

signs of HF?

A

cyanosis, tachycardia, elevated JVP, displaced apex beat
chest signs- bibasal crackles, wheeze
S3 heart sound
narrow pulse pressure

87
Q

what is de novo heart failure?

A

an increase in cardiac filling pressure and myocardial dysfunction usually as a result of ischaemia -> reduces CO -> hypoperfusion -> pulmonary oedema

less common causes are viral myopathy, toxins and valve disease

88
Q

Ix for HF?

A

bloods- FBC, U&E, CRP
CXR- ABCDE
ECHO- pericardial effusion and cardiac tamponade
BNP- >100mg/L indicated myocardial damage

89
Q

mx of acute HF?

A
Oxygen
loop diuretics
opiates
vasodilators- nitrates
inotropic agents
CPAP
ultrafiltration
90
Q

long-term management of HF?

A
4 drugs needed- BASH
Beta blocker
ACE inhibitor
Spironolactone
Hydralazine with nitrates

If symptoms progress- cardiac resynchronisation therapy or digoxin or ivabradine

Diuretics for fluid overload
Annual influenza vaccine
One off pneumococcal vaccine

91
Q

classification of heart failure?

A

New York Heart Association
NYHA class I-
no symptoms, no limitation

NYHA II-
mild symptoms, slight limitation of physical activity

NYHA III-
moderate symptoms, marked limitation

NYHA IC- severe symptoms, unable to carry out any physical activity without discomfort

92
Q

features of chronic heart failure?

A
dyspnoea
cough (pink, frothy sputum)
PND
orthopnoea
wheeze
weight loss
bibasal crackles on examination
signs of RHF: raised JVP, ankle oedema, hepatomegaly
93
Q

Ix of chronic HF?

A
BNP- if >400 refer for specialist assessment and ECHO within 2 weeks)
ECG
CXR
Bloods
urine dipstick
lung function tests
94
Q

cardiac causes of breathlessness?

A
silent MI
cardiac arrhythmia
cardiac tamponade
chronic HF
acute pulmonary oedema
95
Q

pulmonary causes of breathlessness?

A
pneumothorax
pleural effusion 
COPD
asthma
interstitial lung disease
pneumonia
bronchiectasis
96
Q

Mx of PE?

A

well’s score- >4= PE likely
hosp admission for CTPA
if there is a delay in CTPA->

  1. give LMWH and fondaparinux
  2. start warfarin within 24 hours and continue for at least 3 months in unprovoked PE, for active cancer- continue until cure, for pregnancy women, LMWH is continued until the end of pregnancy
  3. thrombolysis 1st line for passive PE with circulatory collapse e.g. hypotension

IVC filters for repeat PEs

97
Q

Ix of PE?

A
Wells score
D-dimer
ECG
CXR
V/Q scan
98
Q

ECG changes in PE?

A

S1Q3T3
large S wave in lead I, large Q wave in lead III and an inverted T wave in lead III

RBBB
sinus tachycardia

99
Q

what is cardiac tamponade?

A

the accumulation of pericardial fluid under pressure

100
Q

causes of cardiac tamponade?

A
malignancy
MI
infection
connective tissue disease
pericarditis
radiation therapy
CKD
101
Q

Beck’s triad for cardiac tamponade?

A

Hypotension
Raised JVP
Muffled heart sounds

102
Q

ECG signs of cardiac tamponade?

A

electrical altercans- alternating amplitude of QRS complex

103
Q

mx of cardiac tamponade?

A

urgent pericardiocentesis

104
Q

what is an aortic dissection?

A

tear in the tunica intima of the wall of the aorta

105
Q

associations with aortic dissection?

same for AAA

A
hypertension
trauma
bicuspid valve
marfans, ehlers danlos
turners and Noonan's syndrome
pregnancy
syphilis
106
Q

features of aortic dissection?

A

chest pain- severe and radiating to back, tearing in nature
aortic regurgitation
hypertension
no ECG changes

107
Q

classification of aortic dissection?

A

Stanford classification
type A- ascending aorta, 2/3 of cases
type B- descending aorta, distal to origin of left subclavian artery

108
Q

mx of aortic dissection?

A

type A- surgical management

type B- conservative, reduce BP with IV labetalol

109
Q

what is an AAA?

A

dilatation of all layers of the arterial wall

110
Q

2 types of AAA?

A

Unruptured- asymptomatic usually

Ruptures- pain in abdomen or back, syncope, shock, collapse, cold and sweating

111
Q

Ix of AAA?

A
Bloods- FBC, clotting, renal function, LFTs, cross match, ESR/CRP
ECG
CXR
USS
CT
MRI
112
Q

mx of unruptured AAA

A

DIAMETER <5.5- treat with USS surveillance and optimise CV risk factors
Diameter >5.5- EVAR (endovascular repair)

113
Q

mx of ruptured AAA?

A

Large bore IV access
group and save and cross match
emergency EVAR or prosthetic graft

114
Q

when are aortic aneurysms screened for?

A

age 65

if negative, rules out for life

115
Q

classification of hypertension?

A

stage 1- clinic >140/90 OR hbpm >135/85

stage 2- clinic >160/100 or HBPM >150/90

stage 3- clinic >180 or clinic diastolic >110

116
Q

causes of hypertension?

A

primary- no identifiable cause
secondary- renal disorders

vascular disorders (coarctation of aorta, renal artery stenosis)

endocrine- primary hyperaldosteronism, phaeochromocytoma, cushings, acromegaly etc

drugs- alcohol, ciclosporin, cocaine, COCP, corticosteroids NSAIDs, erythromycin

connective tissue disorders

117
Q

Ix of hypertension

A

urea and electrolytes: check for renal disease
HbA1c: check for co-existing diabetes mellitus
lipids: check for hyperlipidaemia
ECG
urine dipstick
fundoscopy- hypertensive retinopathy

118
Q

mx of hypertension

A

<55 or T2DM= ACEI
>55 and no T2DM or afro-Caribbean= CCB

combine
add thiazide like diuretic
if K <4.5 - add low-dose spironolactone
if K
>4.5- add alpha or beta blocker

specialist review

119
Q

how do CCBs work?

A

Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction

120
Q

how do thiazide type diuretics work?

A

Inhibit sodium absorption at the beginning of the distal convoluted tubule

121
Q

in intermittent claudication, which arteries correspond to pain where?

A
aortic or iliac artery- hip or buttock pain
thigh pain- iliac or common femoral
upper 2/3 calf- superficial femoral
lower 1/3 calf- popliteal artery
foot- tibial or peroneal artery
122
Q

assessment of intermittent claudication?

A
check peripheral pulses
ABPI- 0.6-0.9= claudication
0.3-0.6= rest pain
duplex USS 1st line
MR angiography prior to any intervention
123
Q

what is diagnostic of critical limb ischaemia?

A

ABPI <0.5

rest pain in foot for more than 2 weeks, ulceration, gangrene

124
Q

features of acute limb ischaemia?

A
1 or more of:
pale
pulseless
painful
paralysed
paraesthetic
'perishing with cold'
125
Q

mx of acute limb ischaemia?

A

quit smoking
treat comorbidities- hypertension, DM, obesity
atorvastatin 80mg
clopidogrel in preference to aspirin
exercise training
severe PAD-> angioplasty, stenting, bypass surgery

126
Q

what are types of tachycardia?

A

narrow complex- QRS <120ms
broad complex- QRS >120ms

narrow complex e.g. sinus, SVT, AF/flutter

broad-complex e.g. VT/VF

127
Q

Mx of bradycardia with haemodynamic compromise

A

give 500mcg IV atropine

128
Q

normal ECG variants in an athlete?

A

sinus bradycardia
junctional rhythm
first degree heart block
wenckebach phenomenon

129
Q

signs of RVH on ECG?

A

Right axis deviation- reaching
negative QRS in lead I
taller QRS in lead III
positive lead II

130
Q

signs of LVH on ECG?

A

Left axis deviation
small QRS lead I
negative lead II and III

131
Q

types of AF?

A

First detected AF
Paroxysmal AF- last less than 7 days
Persistent AF- last greater than 7 days
permanent AF- there is continuous atrial fibrillation which cannot be cardioverted

132
Q

signs and symptoms of AF?

A

palpitations
dyspnoea
chest pain
an irregularly irregular pulse

133
Q

rate control of AF?

A

Rate control- a beta-blocker or rate-limiting calcium channel blocker (cardioselective- e.g. diltiazem)
Digoxin

134
Q

rhythm control for AF?

A

favoured if <65, symptomatic, first presentation, AF, congestive cardiac failure

drugs used- sotalol, amiodarone, flecainide
DC cardioversion (radiofrequency ablation)

heparin if onset AF <48 hours
anticoagulation should be given for 2 weeks prior to cardioversion if AF >48 hours

135
Q

what is the risk of stroke in AF?

A
CHADS2VASc
Congestive heart failure
Hypertension
Age >75
Diabetes
Stroke hx
Vascular disease
Age 65-74
Sex (female)

score >1- consider in males
score >2- high risk, commence on warfarin or DOACS

136
Q

what is atrial flutter?

A

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

137
Q

ECG findings of AF?

A

irregularly irregular pulse
absent P waves
Irregular QRS

138
Q

ECG findings for atrial flutter?

A

p waves absent
saw-tooth appearance
flutter waves may be visible following carotid sinus massage or adenosine

139
Q

types of SVT?

A
  • atrioventricular nodal re-entry tachycardia(AVNRT)- 2 conduction pathways in the AV node
  • atrioventricular re-entry tachycardia (AVRT) - due to an accessory bypass pathway (Bundle of Kent)
  • junctional tachycardia
140
Q

what is the main cause of AVRT?

A

Wolff-Parkinson white syndrome

141
Q

what is WPW syndrome?

A

caused by a congenital accessory conducting pathway between the atria and ventricles

As the accessory pathway does not slow conduction AF can degenerate rapidly to VF

142
Q

possible ECG features of WPW syndrome?

A

short PR interval

‘delta wave’

broad QRS

left axis deviation if right-sided accessory pathway
right axis deviation if left-sided accessory pathway

143
Q

what is a delta wave?

A

slurred broad upstroke of QRS complex

144
Q

mx of WPW syndrome?

A

definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol, amiodarone, flecainide

145
Q

what is ebstein’s anomaly?

A

a congenital heart defect characterised by a low insertion of the tricuspid valve resulting in a large atrium and small ventricle

(atrialisation of RV)

associated with WPW syndrome

146
Q

what is VT?

A

a broad-complex tachycardia originating from a ventricular ectopic focus

-can precipitate to VF

147
Q

what are the 2 types of VT?

A
  • monomorphic VT- most commonly caused by MI

- polymorphic VT- a subtype is torsades de pointes which is precipitated by prolongation of QT interval

148
Q

mx of VT?

A

If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated

Drug therapy:
amiodarone: central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

If drug therapy fails:

  • electrophysiology studies
  • ICDs
149
Q

mx of torsades de pointes?

A

IV magnesium sulphate

150
Q

what are 2 shockable rhythms?

A

pulseless VT

VF

151
Q

what happens in VF?

A

the ventricular muscle fibres contract randomly causing a complete failure of ventricular function

152
Q

RF of VF?

A
coronary artery disease
acute MI
chronic infarction scar
anti-arrhythmic drug administration 
hypoxia
AF
153
Q

ECG findings of VF?

A

no discernible pattern
no QRS
no P or T waves

154
Q

tx of VF?

A

defibrillation and resuscitation

cardioversion

155
Q

what is 1st degree of heart block?

A

PR interval > 0.2 seconds

156
Q

what is 2nd degree heart block?

A
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
157
Q

what is third (complete) degree heart block?

A

there is no association between the P waves and QRS complexes

158
Q

what ECG changes are seen in digoxin?

A

depression of ST, inverted T waves
‘reverse tick’ by sloping of ST segment

this occurs because digoxin blocks the Na/K pump, which increases intracellular Ca

159
Q

what are S1 and S2 heart sounds caused by?

A

S1- closure of mitral and tricuspid valves

S2- caused by closure of aortic and pulmonary valves

160
Q

what is S3 caused by?

A

caused by diastolic filling of the ventricle, gallop rhythm
considered normal if <30 years old

heard in left ventricular failure, constrictive pericarditis, mitral regurgitation

161
Q

what is S4 caused by?

A

occurs just before 1st HS

atrial contraction against a stiff ventricle
may be heard in aortic stenosis, HOCM, hypertension

162
Q

what is the most common cause of infective endocarditis>

A

historically strep viridans, now staph aureus

163
Q

why are BBs and non-dihydropyridine CCBs contraindicated?

A

they are both negatively inotropic and combined affects can cause bradycardia and even asystole

164
Q

warfarin vs DOACS?

A
  • DOACS-
    less monitoring, quicker onset and offset,
    -ve less easier to reverse
165
Q

What is HAS bled score?

A

bleeding risk stratification score for those on oral anticoagulants in AF

Hypertension
Abnormal renal and liver function
Stroke

Bleeding
Labile INRs
Elderly
Drugs or alcohol

166
Q

what monitoring of amiodarone is needed before treatment?

A

TFT, LFT, U&E, CXR prior to treatment

167
Q

what ECG sign can hypothermia show?

A

J waves

168
Q

Which cardio drug can cause ototoxicity?

A

loop diuretics e.g. furosemide

169
Q

ejection systolic murmur?

A

aortic stenosis
pulmonary stenosis, hypertrophic obstructive cardiomyopathy
atrial septal defect, tetralogy of Fallot

170
Q

pansystolic murmur?

A

mitral/tricuspid regurgitation

171
Q

early diastolic murmur?

A
aortic regurgitation (high-pitched and 'blowing' in character)
Graham-Steel murmur
172
Q

Mid-late diastolic murmur?

A
mitral stenosis ('rumbling' in character)
Austin-Flint murmur
173
Q

RFs for infective endocarditis?

A
Prev IE
rheumatic heart disease
prosthetic valves
congenital heart defects
IVDU
piercings
174
Q

causes of IE?

A

staph aureus

streptococcus viridans

175
Q

criteria for IE?

A

Duke’s criteria

176
Q

vascular phenomena for IE?

A
major enmboli
clubbing
splinter haemorrhages
janeway lesions
osler's nodes
roth spots
177
Q

diagnosis of IE?

A

Transthoracic echo
microbiology- 3 samples within 24 hours
bloods

178
Q

mx of IE?

A

Acute presentation – flucloxacillin, gentamycin
Subacute presentation – benzylpenicillin, gentamycin
Prosethetic valve / resistant organism – triple therapy of vancomycin, gentamycin and rifampicin

SURGERY

179
Q

how does a statin work?

A

HMG-CoA reductase inhibitor

180
Q

ECH changes associated with hypothermia?

A
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
181
Q

mx of SVT in a stable patient?

A
  1. Valsalva manoeuvre- Ask the patient to blow hard against resistance, for example into a plastic syringe.
  2. Carotid sinus massage. Massage the carotid on one side gently with two fingers.
  3. Adenosine-works by slowing cardiac conduction primarily though the AV node
  4. An alternative to adenosine is verapamil (calcium channel blocker)
  5. Direct current cardioversion may be required if the above treatment fails
182
Q

bradycardia following an MI is indicative of?

A

heart block

183
Q

what drugs are contraindicated in heart block?

A

beta blockers
non-dihydropyridine CCBs e.g. verapamil
anti-arrhythmic e.g. amiodarone, flecainide

184
Q

what is Dressler’s syndrome?

A

a complication of MI
autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

185
Q

types of broad complex tachycardias?

A

VT, torsades de pointes (prolonged QT), SVT with bundle branch block

186
Q

mx of torsades de pointes?

A

magnesium sulphate infusion

187
Q

types of narrow complex regular tachycardias?

A
sinus tachycardia
atrial flutter
atrial tachycardia
AVNRT
AVRT
188
Q

mx of VT?

A

300mg amiodarone IV over 20-60 mins then 900mg over 24 hours

189
Q

causes of RBBB?

A

can be normal
ASD or congenital disease
PE

190
Q

causes of LBBB?

A

ischaemia
aortic stenosis
hypertension
cardiomyopathy

191
Q

what is partial RBBB?

A

RSR pattern in lead V1 but duration less than 120ms

192
Q

possible ECG features in healthy athletes?

A
sinus bradycardia
junctional rhythm
wandering atrial pacemaker
first degree heart block
Mobitz type 1 2nd degree heart block
193
Q

causes of right axis deviation?

A

normal variant- tall thin people
RVH
lateral MI
WPW syndrome

194
Q

causes of left axis deviation?

A

left anterior hemiblock
WPW syndrome
inferior MI
VT

195
Q

where are Q waves found in old anterior infarcts?

A

V2-4 with T wave inversion