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Year 3 > Block 31 Week 1 > Flashcards

Block 31 Week 1 Flashcards

1
Q

investigations for chest pain?

A
  • ECG
  • troponin
  • lab tests
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2
Q

History for chest pain that suggests cardiac pain?

A
  • central crushing/ heavy pain
  • sudden onset
  • clammy
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3
Q

MI RF?

A
  • FHx
  • hypertension
  • diabetes
  • smoking
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4
Q

what can cause inc troponin?

A
  • loss of BS
  • PE can put strain on R side of heart -> damage
  • inflammation: pericarditis e.g.
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5
Q

PE?

A
  • PE: pain more often pleuritic
  • likely to be SOB
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6
Q

Myocarditis?

A
  • Myocarditis pain is often positional
  • can be pleuritic
  • likely to be ECG changes
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7
Q

heart muscle damage: haemodynamic strain?

A

aortic dissections. sepeis, blood loss, burns, extreme exertion

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8
Q

heart muscle damage: very fast heart rate?

A

fast AF, VT, VF, SVT (palpitations in history)

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9
Q

HM damage: strain within heart?

A

aortic stenosis, obstruction in hypertrophic cardiomyopathy

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10
Q

what is associated w chest pain?

A

aortic stenosis

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11
Q

Takotsubo’s cardiomyopathy?

A
  • Takotsubo’s cardiomyopathy: stressful situation which leads to a ballooning of the apex of the heart -> sig troponin rise and chest pain
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12
Q

HM damage: trauma to heart?

A

e.g. car collision, valve or bypass surgery

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13
Q

type 2 MI?

A
  • MI secondary to another process e.g. sig sepsis - type 2 MI
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14
Q

Sepsis?

A

pyrexial, high white cell count etc

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15
Q

severe aortic stenosis?

A

ejection murmur

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16
Q

mechanisms of blood loss in the heart?

A
  • thrombus formation on underlying diseased coronary arteries - atheromatous plaque
  • coronary artery spasm - transient or peristent vasospasms
  • spontaneous coronary artery dissection
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17
Q

coronary angio vs echocardiogram?

A
  • coronary angiogram - visualisation of coronary arteries (confirms diagnosis)
  • echocardiogram - asesss function of heart muscle
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18
Q

NSTEMI vs STEMI?

A
  • NSTEMI: incomplete occlusion
  • STEMI: restore blood flow within 12 hours
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19
Q

cardiac ischaemic pain?

A
  • central
  • crushing
  • heavy
  • tight band
  • related to exertion
  • relieved by GTN within minutes
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20
Q

descriptors that make u think its not cardiac ischaemic pain

A
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21
Q

Features assoc w cardiac pain?

A
  • clammy
  • nauseaous
  • SOB
  • light headed
  • collapse
  • palpitations
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22
Q

pain history?

A
  • how long
  • constant/ intermittent
  • when was it worse
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23
Q

exacerbating factors for the pain?

A
  • breathing
  • food
  • exertion
  • position
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24
Q

cardiac differentials for chest pain?

A
  • myocarditis
  • takotsubos
  • heart failure
  • pericarditis
  • ACS
  • airtic dissection
  • severe aortic stenosis
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25
Q

resp differentials for chest pain ?

A
  • pleuritis
  • pneumothorax
  • PE
  • pulm hypertension
  • asthma exacerbation
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26
Q

GI differentials for chest pain?

A
  • GORD
  • oeseophagitis
  • oeseophageal spasm
  • gastritis
  • gastric ulcer
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27
Q

MSK differentials for chest pain?

A
  • rib fractures
  • costochondritis
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28
Q

other differentials for chest pain?

A
  • panic attacks
  • somatisation
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29
Q

ripping tearing severe central chest pain radiating to the back ->

A

aortic dissection

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30
Q

sharp positional pain worse when lying flat and eased when sitting ->

A

pericarditis, myocarditis

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31
Q

central, heaving crushing pain worse on exertion, radiation to jaw or arms, clammy, sweaty, nausea ->

A

MI

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32
Q

Sharp pain, worse on inspiration, SOB, D dimer positive ->

A

PE

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33
Q

Central crushing pain Ix

A
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34
Q

angina?

A
  • lumen diameter reduced by around 50% so coronary blood flow is unable to respond to an inc in metabolic demand
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35
Q

NSTEMI/ unstable angina

A
  • resting flow affected when lumen diameter reduced by ~80%
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36
Q

STEMI?

A
  • sudden complete occlusion
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37
Q

Ix for SOB + chest pain

A
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38
Q

angina Ix results

A
  • ECG can have ST depression and/or T wave inversion
  • troponin negative
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39
Q

NSTEMI Ix results?

A
  • ECG can be normal or have ST depression and or T wave inversion
  • troponin positive
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40
Q

STEMI results?

A
  • troponin positive
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41
Q

GI bleed and type 2 MI?

A
  • massive GI bleed can precipitate MI from hypovolemia and myocardial hypoerfusion
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42
Q

Causes of MI

A
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43
Q

angina pain?

A
  • chest pain on exertion
  • less severe partial occlusion w plaque
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44
Q

unstable angina characteristic pain?

A
  • chest pain on progressively less exertion and now episodes at rest
  • partial occlusion
  • increasing plaque and thrombus
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45
Q

NSTEMI pain?

A
  • sudden onset chest pain at rest
  • partial occlusion
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46
Q

STEMI pain?

A
  • sudden onset chest pain at rest
  • total occlusion
  • plaque rupture and thrombus
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47
Q

types of MI?

A

Angina and NSTEMI can have ST depression/ T wave inversion

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48
Q

differentials for angina/ MI?

A
  • coronary artery spasm
  • SCAD
  • Takosubo’s
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49
Q

X rays?

A
  • different tissues attenuate the beam to varying degrees depending on atomic constituents
  • The image starts all white. If x-rays reach the detector that part of the image turns black.
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50
Q

Why are bones white on X ray?

A
  • bones have a high atomic denstity so white as lots of X rays are abs so only a few pass through
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51
Q

heart on an XR?

A
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52
Q

Lungs on an XR

A
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53
Q

Consolidation?

A
  • radiological sign
  • alveoli and small airways fill up with material
  • Larger airways remain air-filled giving rise to an ‘air bronchogram’ sign
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54
Q

What can give rise to consolidation on a CXR (3)

A
  • Pus (e.g. in pneumonia)
  • Fluid (e.g. in pulmonary oedema)
  • Blood (e.g. in traumatic contusions)
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55
Q

e.g. of consolidation

A
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56
Q

air bronchogram?

A
  • black areas within the area of inc density
  • these are larger airways that remain air filled so you can see them clearly
  • key part of consolidation
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57
Q

lung collapse?

A
  • can be partial - collapse of one lobe of the lung
  • or total which is collapse of an entire lung
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58
Q

lung collapse - compression?

A

(e.g. due to fluid or air in the pleural space around the lung in an effusion or pneumothorax respectively)

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59
Q

Lung collapse - obstruction?

A
  • or obstruction of a bronchus e.g. by tumour or an inhaled foreign body (where the lung distal to the obstruction will collpased)
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60
Q

Lung collapse in a child?

A
  • lung collapse in a child is often due to inhalation of a foreign body or mucus obst in asthma
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61
Q

lung collapse in an adult?

A
  • Lung collapse in an older person raises concern for an underlying tumour (e.g. primary lung cancer) and further investigation is often required (e.g. with CT and/or bronchoscopy).
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62
Q

main features of collapse?

A
  • area of homogenous increased density without air bronchograms (vs consolidation).
  • There are no air bronchograms as all the airways are collapsed distal to the obstruction and do not contain air.
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63
Q

sail sign?

A
  • left lower lobe collapse
  • creates triangle of increased density behidnt he heart
  • makes it look like there are 2 heart borders
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64
Q

CT of left lower lobe collapse?

A
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65
Q

pleural effusion?

A
  • accumulation of fluid in the pleural space
  • appears as an area of homogenous increased density (whiter than the normal lungs)
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66
Q

pleural effusion CXR?

A
  • If the CXR is taken with the patient sat up or stood up, the fluid will settle dependently and will obscure the diaphragm.
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67
Q

bilateral vs unilateral Pleural effusion?

A
  • It can be unilateral (typical in malignant causes) or bilateral (typical in heart failure)
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68
Q

pleural effusion x ray

A
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69
Q

P effusion causes

A
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70
Q

V large pleural effusion

A
  • an effusion as large as this is v concerning for a malignant cause like lung cancer, mesothelioma etc
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71
Q
A
  • complete collapse of the left lung
  • signs of colume loss in the left hemithorax - trachea is pulled to the left and the D is pulled up - stomach bubble seen high on left side
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72
Q
A
  • massive left pleural effusion
  • this is bc there are signs of increased volume in the left hemithorax due to the fluid - trachea and heart are shifted away to right side
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73
Q

How to differentiate large effusion from collapse?

A
  • Working out whether there is volume loss or increased volume in the hemithorax is key to differentiating between a large effusion or collapse.
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74
Q

PLC on CXR?

A
  • primary LC appears as a solid mass on CXR usually
  • This will usually not contain air bronchograms (like consolidation does)
  • Sometimes you will not see the actual mass but will see the result of the mass such as collapse of the lung or one lobe of the lung, or a pleural effusion.
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75
Q

CXR vs CT for lung cancer

A
  • CXR usually done as first Ix as it is readily available and involves little radiation exposure
  • CT is more sensitive for lung cancer than CXR - so if high clinical suspicion do a CT
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76
Q

lung cancer CXR?

A
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77
Q

Causes of PF

A
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78
Q

Severe fibrosis scan

A
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79
Q

cardiomegaly

A
  • normal cardiothoracic ratio: 50%
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80
Q

HF features on CXR?

A
  • cardiomegaly
  • pleural effusions (due to fluid leak into the pleural space)
  • septal thickening - due to fluid leak into the intersitial space
  • consolidation due to fluid leak into the alveoli
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81
Q

HF signs are usually?

A

bilateral

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82
Q

HF CXR ?

A
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83
Q

Summary of HF CXR?

A
  • cardiomegaly,
  • small pleural effusions,
  • some septal thickening
  • and bilateral consolidation
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84
Q

CHD incidence?

A
  • 1 in 6 male deaths and 1 in 9 female deaths
  • most common cause of death in under 75s in the UK
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85
Q

ACS cause?

A
  • ACS are caused by rupture of lipid rich atheroma plaques.
  • -> platelet adhesion
  • activation and thrombin activation with resultant occlusion / partial occlusion of the coronary artery and ischaemia/infarction.
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86
Q

stable angina cause?

A
  • stable angina is usually caused by plaques which sig reduce lumen of the artery so ischemia occurs on exertion
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87
Q

occluded artery image

A
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88
Q

history taking?

A
  • the character, duration, severity and radiation of the pain.
  • relieving/exacerbating factors
  • associated symptoms (eg nausea)
  • and consider differential diagnoses (eg varying with respiration - pleurisy or pericarditis, upper GI symptoms such as indigestion, weight loss).
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89
Q

PMH/ RF for CAD?

A
  • previous vascular disease
  • RF for coronary artery disease - smoking, diabetes, obesity, hypertension, FHx
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90
Q

Co-morbidities that can cause a contra-indication for ACS meds?

A
  • Any potential co-morbidities that might indicate a contra-indication to the medications required for ACS treatment eg recent GI bleed when taking aspirin therapy
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91
Q

cardiac examination

A
  • haemodynamic status - pulse, BP, resp rate, O2 sats
  • signs of cardiac failure:
  • crackles in the lung bases
  • elevated JVP
  • gallop rhythm
  • peripheral oedema
  • underlying cardiac disease e.g. murmur of aortic stenosis
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92
Q

Ix of CAD?

A
  • make the diagnosis (ECG and cardiac enzymes)
  • exclude exacerbating factors (eg anaemia)
  • identify complications (eg pulmonary oedema on CXR)
  • evaluate left ventricular function (echocardiography)
  • in some cases exclude other diagnoses (eg amylase-acute pancreatitis)
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93
Q

meds for CAD?

A

Antiplatelets and statins

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94
Q

Mx of CAD?

A
  • meds - antiplatelets, statins
  • pain relief e.g. opiates + anti-emetics
  • nitrates - sublingal GTN or IV infusion
  • consider oxygen
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95
Q

STEMI Mx?

A
  • PCI
  • aspirin 300mg stat
  • proximitiy to defibrillator requiredc
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96
Q

complications of AMI?

A

eg: arrhythmia, cardiac arrest, LV failure, recurrent ischaemia

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97
Q

All AMI ppts should undergo assessment of?

A

LV function prior to discharge - echo

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98
Q

PPCI?

A
  • aims to restore blood flow by using a soft wire to cross the occluded coronary segment and perform intervention to open the narrowing
  • thrombus may be extracted and procedure relies on pharm - anti-thrombotic and anti-platelets to treat the thrombus
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99
Q

What happens after PPCI?

A
  • stent inserted to maintain vessel lumen then dual anti-platelet therapy required
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100
Q

nstemi - early Tx w?

A
  • early treatment with aspirin, statin, and low molecular weight heparin to reduce the risk of AMI/death
  • second anti-platelet agent should also be given (eg clopidogrel, ticagrelor or prasugrel)
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101
Q

NSTEMI - consider IV?

A
  • Consider IV glycoprotein IIb/IIIa inhibitor for high risk/ unstable ppts
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102
Q

NSTEMI - anti-ischaemics?

A

BBs, nitrates (CCBS, nicorandil, ivabradine, ranolazine)

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103
Q

ACS Tx pathway

A
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104
Q

Ix for MI?

A
  • Identify risk factors for atheroma
  • eg glucose and cholesterol
  • Identify factors that exacerbate angina
  • eg haemoglobin (anaemia), thyroid function (hypothyroid / thyrotoxicosis)
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105
Q

CAD likelihood

A
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106
Q

Identify cardiac abnormalities

A
  • ECG (often normal in patients with angina)
  • Echocardiogram if needed (eg suspicion of LV dysfunction, cardiac murmur)
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107
Q

rapid access chest pain clinic?

A
  • those with recent onset angina should be seen within 2 weeks of referral in a rapid access chest pain clinic
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108
Q

Tx of angina - anti-ischaemics?

A

e.g beta-blockers, calcium channel blockers, nicorandil, ivabradine, ranolazine, long-acting nitrates

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109
Q
A
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110
Q

angina - Additional treatment to reduce the risk of MI/death?

A
  • aspirin, statins
  • management of diabetes and hypertension, smoking cessation, encourage exercise (assuming symptoms are stable)
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111
Q

angina - symptoms despite medical therapy

A
  • those w ongoing symptoms despite medical therapy should be considered for revascularization - either PCT or CABG
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112
Q

EA of heart?

A
  • EA starts at SA node
  • spreads through atrium to AV node where it is delayed
  • travels down BoH
  • down right and left bundle branches
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113
Q

P wave?

A

electrical signal from SA node spread through atria and cause them to depolarise

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114
Q

PR segment =

A

time signal travels through AV node

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115
Q

Q wave =

A

depolarisation of intraventricular septum

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116
Q

R wave =

A

depolarisation of bulk of ventricle

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117
Q

S wave =

A

last phase of ventricular depolarisation

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118
Q

ST segment?

A

plateau in myocardial action potential (when ventricles contract and pump blood)

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119
Q

T wave?

A

ventricular repolarisation

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120
Q

Segments and waves on an ECG

A
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121
Q

Q R and S waves

A
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122
Q

Basic ECG

A
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123
Q

Segment on an ECG?

A

Lines that connect waveforms

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124
Q

Which segment is used as the baseline on an ECG?

A
  • TP segment is the least affected by pathology so can be used as the baseline within the ECG
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125
Q

QRS interval?

A
  • QRS = duration of QRS complex alone, should be less than 120ms long
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126
Q

P-R interval?

A
  • PR interval = 120-200ms
  • P wave and PR segment
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127
Q
A
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128
Q

QT interval?

A
  • QRS + ST segment + T waveform
  • dependent on heart rate
  • < 1/2 RR
129
Q

RR interval =

A
  • everything within 1 cardiac cycle
130
Q

ECG limb leads?

A

Right arm: red
Left arm: yellow arm
Left leg: green
Right leg: black

131
Q

aVR, aVL and AVF leads

132
Q

cardiac axis

133
Q

aVR, avL and avF?

A
  • avR: right shoulder
  • avL: left shoulder
  • avF: floor
134
Q

lead 1?

A
  • positive P wave as a positive deflection reflects electrical activity going towards the positive pole
  • R and T wave also positive
135
Q

lead 2 ?

A
  • aligned w electrical activity of atrial and ventricular depolarisation
  • so strongly positive P wave and R wave in a normal lead 2 - tall waves
136
Q

lead aVF?

A
  • Positive P wave and R wave
137
Q

Which leads do you see positve P and R waves in?

A
  • positive P waves and R waves in leads 1, 2, aVF
139
Q

aVR?

140
Q

aVL?

141
Q

v1-v6

142
Q

I, II, III and A leads

143
Q

aVR waves?

A
  • Reads opposite direction to electrical activity of the heart
  • so the waves are upside down!!
143
Q

aVL?

A
  • Reads at right angles to EA
144
Q

Rate on an ECG?

A
  • 1 small box = 40ms
  • 1 big box (5 small boxes) = 200ms
  • 5 big boxes = 1 second
147
Q

How to calculate rate on an ECG?

A
  • rhythm strip (at the bottom) is often lead 2
  • use this for rate
  • 300 big big boxes in 1 minute
  • 300/ number of big boxes between the 2 QRS complexes e.g. 300/4 = 75 for a regular rhythm
148
Q

caculating rate on an irreg rhythm?

A
  • for an irreg rhythm take number of complexes in the 10s x 6 to get the rate
149
Q

QRS axis?

A

represents the average direction of electrical activity in the heart during ventricular depolarisation (projected onto frontal plane)

150
Q

boxes on an ECG

151
Q

Normal cardiac axis

154
Q

LAD leads

A
  • positive lead 1, negative lead 2
  • negative AVF
156
Q

positive, negative and isoelectric leads

157
Q

Leads in RAD?

A
  • Negative lead 1
  • positive in lead aVF
158
Q

normal axis =

A

positive in both lead 1 and lead aVF

159
Q

LAD vs RAD

A
  • LAD: positive in lead 1 and RAD is negative in lead 1
  • LAD is negative in AVF and RAD is positive in aVF
160
Q

LAD summary

A
  • positive in lead 1
  • negative in lead 2
  • negatIve in aVF
161
Q

RAD summary

A
  • negative in lead 1
  • positive in aVF
162
Q

normal vs right vs left axis

163
Q

causes of LAD

164
Q

Causes of right axis

165
Q

Non pathological factors affecting QRS?

A
  • Short and obese: QRS close to 0
  • young age: right axis at birth
  • tall and thin: QRS close to +90
166
Q

NSTEMIs?

A
  • INCOMPLETE OCCLUSION
  • but enough to cause some myocardial ischaemia
  • Angiogram, but does not need to be within 12hours
  • troponin +ve
167
Q

STEMI?

A
  • complete occlusion
  • angiogram ASAP within 12 hrs (PPCI)
  • trop +ve
168
Q

type 2 MI?

A
  • treat sepsis: blood loss or other prec factors
  • troponin +ve
169
Q

NSTEMI ECG changes?

A
  • may have ST depression and/or T wave inversions
170
Q

STEMI vs NSTEMI ECG

171
Q

Arteries of the heart

172
Q

What do you see in a STEMI?

A
  • ST elevation in 2 or more leads
  • may have ST depression and or T wave inversions
173
Q

ECG changes that occur in minutes?

A
  • T wave inversion and hyperacute T waves
174
Q

ECG changes that occur in minutes/ hours

A
  • ST depressions and elevations
175
Q

ECG changes that occur in hours - days?

A
  • pathological Q wave
176
Q

Right dominant circulation

177
Q

left dominant circ?

178
Q

LAD supplies the?

A
  • Supplies anterior wall of left ventricle
  • Supplies intraventricular septum
  • Supplies apex
178
Q

what does the circumflex artery supply?

A
  • Supplies the left atrium
  • Supplies lateral wall of left ventricle
178
Q

What are the lateral leads?

A
  • lateral wall
  • circumflex artery
  • 1
  • aVL
  • V5 and V6
178
Q

what does the RCA supply?

A
  • Supplies right ventricle
  • Supplies the right atrium
  • Usually supplies posterior descending artery and therefore the posterior and inferior walls of left ventricle
180
Q

What are the inferior leads?

A
  • 2
  • 3
  • aVF
  • posterior descending artery, inferior wall
181
Q

What are the anterior leads?

A
  • anterior wall
  • left anterior descending (LAD)
  • V3 and V4
182
Q

septal leads?

A
  • intraventricular septum
  • LAD
  • V1 and V2
183
Q

Large anterior MI?

A

(LAD) can give ST in V2 - V5 or more

184
Q

Laterl wall MI?

A
  • High lateral wall (I; aVL) can be supplied by either LAD or Cx
  • V1& V2 can show posterior changes
185
Q

j point =

A

the junction between QRS complex and the ST segment

186
Q

diffuse J point

187
Q

Clear J point

188
Q

concave and convex ST elevation

189
Q

STEMI criteria?

A
  • ST elevation >1mm in contigous limb leads
  • ST elevation >2mm in contigous chest leads
  • new LBBB
190
Q

chostochondritis?

A
  • inflammation of rib cartilage in chest wall
  • one of the most common chest pains in adults
  • self limiting and benign
191
Q

chostochondritis pain?

A
  • sharp aching or pressure like pain in the chest wall
  • worsens w deep breath, cough, activity involving upper body
  • and lying on affected side
192
Q

where is chostocondritis pain typically felt?

A
  • noted in more than 1 location and typically felt between 2nd and 5th ribs
193
Q

common causes of chest pain

194
Q

Pulm hypertension pain?

A
  • pressure pain
  • substernal
  • dysponea, sign of inc venous pressure including oedema and venous distention
195
Q

pneumonia or pleuritis pain?

A
  • pleuritic pain
  • unilateral often localised
  • dyspnea, cough, fever, occassional rub
197
Q

spontanoue pneumothorax pain?

A
  • sudden onset: several hours
  • pleuritic pain
  • lateral to side of pneumothorax pain
  • dyspnea, dec breath sounds on side of pneumothorax
198
Q

oesophageal reflux ?

A
  • 10-60 mins onset
  • burning pain, substernal/ epigastric
  • worsened by post prandial recumbency
  • relieved by antacids
199
Q

oesophageal spasm pain?

A
  • 2-30 min onset
  • pressure, tightness burning
  • retrostrenal pain
  • can closely mimic angina
200
Q

GB disease pain?

A
  • prolonged onset
  • burning/ pressure pain
  • epigastric/ RUQ pain, substernal
  • may follow meal
201
Q

serious causes of pleurtic chest pain?

A
  • aortic dissection
  • malignant pleural effusion
  • MI
  • pericarditis
  • pneumonia
  • pneumothorax
  • PE
  • TB
202
Q

Aortic dissection pain?

A
  • tearing sensation
  • pain radiates to back/ abd
  • most severe at onset
203
Q

physical exam of AD?

A
  • BP/ radial pulse discrepency
  • aortic murmum
  • possible cardiac tamponade
204
Q

test for AD?

A

D-dimer often elevated

205
Q

malignant P effusion red flags?

A
  • history of malignancy
  • night sweats
  • older age
  • tobacco use
  • weight loss
206
Q

physical exam findings in MPE?

A
  • Locally decreased breath sounds
207
Q

CXR for MPE?

A

unilateral or bilateral effusions

208
Q

MI red flags?

A
  • angina
  • headache
  • arm/ neck pain
  • nausea/ vomiting
209
Q

MI examination findings?

A
  • diaphoresis
  • hypotension
  • third heart sound
  • CXR often normal
210
Q

pericarditiis red flags?

A
  • recurrent or recent viral infection
211
Q

pericarditis exam findings?

A
  • diffuse conccave upward ST segments
  • PR segment depression w/o T wave inversion
  • positional chest pain
212
Q

Ix results for pericarditis?

A
  • possible cardiomegaly
  • ECG w diffuse ST elevation
213
Q

PE red flags?

A
  • acute onset dysponea
  • history of venous thrombosis
  • history of malignancy
  • unilateral leg swelling
214
Q

exam findings for PE?

A
  • Hypotension
  • hypoxia
  • sinus tachy
  • resp distress
215
Q

TB red flags?

A
  • exposure
  • haemoptysis
  • fever
  • night sweats
  • weight loss
216
Q

imaging results TB?

A
  • Often consolidation
  • lymphadenopathy
  • and/or unilateral pleural effusion
  • cavitation common
217
Q

serious causes of chest pain

218
Q

pleurodynia?

A
  • refers to sudden and severe chest or upperabdominal pain, typically caused by an enteroviral infection (e.g., coxsackie A, coxsackie B, andechovirus).
  • Pleurodynia is most commonly caused by group Bcoxsackie virusand typically occurs as an epidemic
219
Q

features of pleurodynia?

A
  • severe intermittent pleuritic chest pain or upper abdo pain from inflammation of ICMs
  • most common in younger adults and children
  • after exposure to enterovirus, typically unilateral
220
Q

pleurodynia pain?

A
  • knife like spasms lasting 15-30 mins
  • sometimes profuse sweating
221
Q

pleurodynia assoc features

A
  • fever, malaise, headaches, cough, sore throat, muscle aches and pains
223
Q

GORD RF?

224
Q

oesophageal cancer symptoms?

A
  • Constitutional symptoms: fevers, anorexia, lethargy, weight loss
  • Dysphagia
  • weight loss
  • bleeding - haematemesis and melaena
  • pain: typically retrosternal
225
Q

Other Sx of OC?

A
  • aspiration - cough, SOB, fever
  • hoarseness - recurrent laryngeal nerve
226
Q

Signs of OC?

A
  • Lymphadenopathy: if local tumour spread
  • Cachexia
  • Pallor: due to anaemia
  • Hepatomegaly: if metastatic spread
227
Q

Classical features of GORD?

A
  • classically occurs after meals and is made worse by lying down or bending forwards
228
Q

signs and symptoms of GORD?

A
  • Regurgitation
  • Dyspepsia
  • Chest pain
  • Dysphagia(difficulty swallowing)
  • Odynophagia(painful swallowing)
229
Q

other features of GORD?

A
  • Cough
  • Hoarse voice
  • Nausea and/or vomiting
230
Q

acute pericarditis ?

A
  • acute-onset chest pain and characteristic ECG features (e.g. saddle ST elevation). Multiple aetiologies.
  • Self-limiting without significant complications in 70-90% of cases.
231
Q

Chronic pericarditis?

A
  • long standing inflammation > 3 months usually following acute episode
  • Complications include chronic pericardial effusion and constrictive pericarditis due to scarring.
232
Q

idiopathic pericarditis?

A
  • sig prop of cases
233
Q

viral pericarditis?

A
  • short lived lasting 1-3 weeks
  • Often due to coxsackievirus B.
  • Variety of other viruses implicated (e.g. influenza, echovirus, adenoviruses, enterovirus, etc)
234
Q

bacterial pericarditis?

A
  • May occur due to haematogenous spread, extension from pulmonary infection or as complication of endocarditis or trauma.
235
Q

TB?

A
  • high prevalence areas or high risk patients e.g. immunodeficiency
  • More insidious onset.
  • High-risk of chronic pericarditis and constrictive complications.
236
Q

Pericarditis - systemic disease?

A
  • underlying systemic inflammatory disease (e.g. rheumatoid arthritis). Features of systemic disease on clinical assessment.
  • May complicate chronic kidney disease (e.g. uraemic pericarditis), hypothyroidism or post-myocardial infarction
237
Q

other causes of pericarditis?

A

drugs, radiotherapy and trauma

238
Q

ACS?

A
  • medical emergency
  • atherosclerosis is the most sig aetiological factor
239
Q

STEMI definition?

A

ST-segment elevation or new-onset left bundle branch block and raised troponins.

240
Q

NSTEMI definition?

A

Non-specific signs of ischaemia or normal ECG, raised troponins.

241
Q

UA definition?

A

Characteristic clinical features, non-specific signs of ischaemia or normal ECG, normal troponins.

242
Q

acs is typically triggered by?

A

rupture of an atheromatous plaque in the coronary arterial wall - atherosclerosis

243
Q

CAD =

A

rupture of an atheromatous plaque in the coronary arterial wall - atherosclerosis

244
Q

Modifiable RF for atherosclerosis?

A
  • ​High cholesterol
  • Hypertension
  • Smoking
  • Diabetes
  • Obesity
245
Q

Non modifiable RF for atheroscleroosis ?

A
  • Age
  • Family history
  • Male sex
  • Premature menopause
246
Q

other causes of ACS/ infarction ?

A
  • emboli and dissection -> vessel occlusion
  • anaemia - oxygen supply/ demand mismatch - not total occlusion, just a lack of perfusion which leads to necrosis and troponin rise
247
Q

causes of coronary occlusion ?

A
  • Vasculitis(e.g. Kawasaki disease)
  • Coronary vasospasm(e.g. spontaneous, cocaine)
  • Coronary dissection
248
Q

causes of changes in oxygen demand/ delivery -> ACS

A
  • Anaemia
  • ​Hyperthyroidism
  • Severe sepsis
249
Q

Pathophys of atherosclerosis?

A
  • endothelial dysfunction
  • LDL accumulation -> ROS
  • plaque formation
  • plaque rupture
250
Q

1: endothelial dysfunction?

A
  • This causes a local inflammatory response. If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of LDL.
  • These become oxidised by local waste products creating reactive oxygen species (ROS).
251
Q

2: plaque formation?

A
  • endothelial cells attract monocytes which phagocytose the LDLs -> foam cells and fatty streaks
252
Q

3: plaque rupture?

A
  • continued inflammation triggers SM cell migration
  • This forms a fibrous cap, which together with the fatty streaks, develops into anatheroma.
253
Q

how does plaque rupture cause vessel narrowing?

A
  • The top of the atheroma forms a hard plaque.
  • This may rupture through its endothelial lining exposing a collagen-rich cap.
  • Platelets aggregate on this exposed collagen forming athrombusthat may occlude or severely narrow the vessel.
  • Alternatively, the thrombus may break lose,embolisingto infarct a distant vessel.
254
Q

ECG and tropnin changes to distinguish the 3 causes of ACS

255
Q

CFs of ACS?

A
  • Chest pain > 15 minutes: central crushing or pressing pain +/- radiation to neck or arm
  • Shortness of breath
  • Sweating
  • Nausea and vomiting
  • Palpitations
256
Q

Signs of ACS?

A
  • Pale
  • Clammy
  • Tachycardia
  • Cardiac failure(e.g. pulmonary oedema, hypotension)
257
Q

ST elevation on an ECG?

A
  • may occur due to AMI or pericarditiis
  • can also be caused by coronary vasospasm, benign early repolarisation, BBB and ventricular aneurysm
258
Q

ST elevation vs depression

259
Q

Ix of ACS?

A
  • ABCDE + history and examination
  • ECG: ST elevation or LBBB
  • if absent look for other features of ischaemia e.g. ST depression, T wave inversion
  • cardiac enzymes: troponin
260
Q

3 ECG features of ischemia?

A
  • ST elevation
  • ST depression
  • T wave inversion
261
Q

ST elevation?

A

seen in STEMI, may be evidence of reciprocal ST depression

262
Q

ST depression?

A

more specific sign of ischaemia than T wave changes. Seen in NSTEMI/UA. Also seen as reciprocal change with ST elevation

263
Q

T wave inversion =

A

less specific sign of ischaemia. Multiple causes. Seen in NSTEMI/UA and as part of the natural evolution of a STEMI over days.

264
Q

ST depression?

A
    • May occur due to acute myocardial ischaemia or as a reciprocal change to ST elevation.
  • Other causes can include electrolyte disturbances, digoxin effect and bundle branch blocks.
265
Q

coronary artery territories?

266
Q

T wave inversion - fixed?

A
  • feature of myocardial ischamia, even in absence of ST changes
  • T wave inversion may befixed, which is usually associated with aprevious ischaemic eventand associates with Q waves.
267
Q

dynamic T wave inversion?

A

Alternatively, T wave inversion may bedynamic, which is associated with&acute myocardial ischaemia.

268
Q

Anteroseptal STEMI?

269
Q

lateral STEMI ?

A

V5-V6, I, aVL

270
Q

inferior STEMI?

A

II, III, aVF

271
Q

Posterior STEMI?

A

no ST elevation on routine ECG. Dominant R wave V1. May be ST elevation by placing posterior leads V7-V9.

272
Q

natural evolution of a STEMI?

A
  • Minutes to hours: hyperacute T-waves
  • 0-12 hours: ST-elevation
  • 1-12 hours: Q-wave development
  • Days: T-wave inversion
  • Weeks: T-wave normalisation and persistent Q-waves
273
Q

STEMI progression

A

hyperacute T waves -> ST elevation -> Q waves -> T wave inversion -> T wave normalisation

274
Q

CXR in ACS?

A

may be signs of HF

275
Q

Echo for ACS?

A
  • reduced EF and or valvular pathology
    • also useful to look for regional wall motion abnormalities
276
Q

CT pulm angiography in ACS?

A

if PE is suspected or needs to be excluded

277
Q

CT angiography in ACS?

A

if aortic dissection suspected or needs to be excluded

278
Q

ACS Mx - MONA?

A
  • morphine + anti-emetic
  • oxygen - if sats under <94% or under <88% in hypercapnic resp failure
  • nitrates
  • aspirin 300mg
279
Q

STEMI management also includes…

A
  • emergency reperfusion required to restore coronary flow
280
Q

PPCI criteria?

A
  • Patients diagnosed with a STEMI, who presentwithin 12 hours of onset of chest pain, should be referred foremergencycoronary angiography +/- primary percutaneous coronary intervention(PCI).
  • This should occurwithin 120 minutesof being diagnosed with ST elevation
281
Q

coronary angiography and PPCI involves?

A
  • coronary angiography involves insertion of a catheter via the femoral or radial artery
  • From here, the catheter can be passed to the coronary artery vessels with x-rays for guidance and contrast injected.
  • During the procedure a balloon catheter can be inserted to open up a blockage. A stent can be then be inserted into the blocked artery.
282
Q

Fibrinolysis criteria?

A
  • If PCI is unable to be performed within 120 minutes then fibrinolytic agents should be considered (e.g. alteplase) while arranging transfer to a PCI centre. Coronary angiography +/-
283
Q

when should PCI be performed after fibrinolysis?

A
  • PCI should be performed in the following 2-24 hours after fibrinolysis and may be required more urgently if patients develop worsening symptoms (e.g. worsening pain, haemodynamic instability, cardiac arrest).
284
Q

which medications should the patient be put on prior to PCI?

A
  • Patients should be initiated on aspirin and asecond anti-platelet drug prior to PCI.
  • This is usually ticagrelor
  • clopidogrel can also be used if there’s a high bleeding risk or prasugrel
285
Q

Post PCI drugs?

A
  • The combination of aspirin and a second anti-platelet agent is referred to as dual anti-platelet therapy (DAPT) and this should be continued for 12 months post-PCI.
286
Q

antithrombotic agents in PCI?

A
  • unfractionated or LMWH
  • usually given at time of PCI
  • or glycoprotein IIb/IIIa inhibitors(e.g. tirofiban) may be given at the time of PCI in the presence of a high thrombus burden.
287
Q

Anti-coags in NSTEMIS?

A
  • Additional antiplatelet agent(e.g. clopidogrel, ticargrelor)
  • Antithrombotic agent(e.g. fondaparinux, UFH)
  • GRACE risk of <1.5% treated w anti-platelet therapy
288
Q

Low risk NSTEMI patients can be started on?

A

aspirin only whilst awaiting further Ix

289
Q

NSTEMI - ppts should be subsequently initiated on DAPT and fondaparinux if:

A
  • Significant delta change in troponin
  • Worsening/recurrent ischaemic pain
  • Deterioration(e.g. cardiogenic shock, arrhythmia, dynamic ECG changes)
290
Q

other Ix?

A
  • Transthoracic echocardiography
  • Stress echocardiography:
  • Cardiac MRI
  • CT coronary angiography
291
Q

transthoracic echo?

A

assessing for evidence of ischaemia (e.g. RWMAs, LV dysfunction). Also useful to investigate alternative pathologies.

292
Q

stress echo?

A

can be considered if negative troponins, normal ECG and chest pain free for several hours.

293
Q

cardiac MRI?

A

can assess both perfusion and wall motion abnormalities. Able to detect recent infarction and assess for previous scars.

294
Q

CT coronary angiography?

A

good at excluding coronary artery disease by visualisation of coronary anatomy.

295
Q

Treatment summary for NSTEMIs/ UA?

A
  • B- Beta-blockers (unless contraindicated)
  • A- Aspirin (300 mg loading, then 75 mg once daily)
  • T- Ticagrelor, alternatively clopidogrel if high bleeding risk
  • M- Morphine (titrate for analgesia)
  • A- Antithrombotic agent (Fondaparinux 2.5 mg subcutaneous unless contraindicated)
  • N- Nitrates (sublingual nitrates to relief pain - consider infusion if ongoing pain)
296
Q

GRACE scoring?

A
  • estimates 6 month mortality risk in patients w NSTEMI/ UA
297
Q

LTM of ACS

A

modifiable risk factors: smoking, dietary changes, exercise, reduce alcohol consumption

298
Q

drugs used to reduce risk after an MI?

A
  • DAPT
  • BBs
  • high dose statin
  • ACEi
  • consider mineralcorticoud antagonist
299
Q

DAPT after an MI?

A

(e.g. aspirin and clopidogrel): should be continued for one year. Vital if had PCI to prevent in stent thrombosis.

300
Q

What can be used instead of an ACEi after an MI?

A

Angiotensin receptor blocker can be an alternative if side-effects or inlolerant to ACE inhibitor)

301
Q

Mineralcorticoid antagonist after an MI?

A

reserved for patients with LV dysfunction (i.e. heart failure) following MI.

302
Q

stemi managemrnt

303
Q

NSTEMI management

304
Q

barriers to rapid diagnosis of AMI?

A
  • atypical presentation e.g. elderly with comorbitiies or women
  • -> lack of knowkedge - health literacy
  • can present like indigestion -> GP
305
Q

Barriers to arrival at hospital for an MI?

A
  • distance
  • access to transport
  • availibility of ambulances
306
Q

Barriers to early diagnosis and Tx of an MI?

A

availability of proper treatment, staff shortages, waiting lists

307
Q

methods of reducing delay?

A
  • patient education on atypical presentations
  • early ECG/ troponin on arrival
  • early diagnsosis for STEMI for PPCI/ fibrinolysis
308
Q

? pain is typical of gastro-oesophageal reflux disease

A

Nocturnal burning chest pain typical of gastro-oesophageal reflux disease

309
Q

A 24 year old woman with exertional breathlessness, dizziness, chest discomfort and central cyanosis.

A

Pulmonary arterial hypertension

310
Q

anti-HTN to avoid in gout?

A

Thiazides reduce the clearance of uric acid, and raise the levels of uric acid in the blood. Hence they are prescribed with caution in patients with gout or hyperuricemia. Loop diuretics also produce this problem but less so.

311
Q

Pickwickian syndrome?

A

Obesity hypoventilation syndrome (also known as Pickwickian syndrome) is a condition in which severely overweight people fail to breathe enough whilst asleep, resulting in high blood carbon dioxide (CO2) levels.

Year 3 (45 decks)

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