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Year 3 > Week 5 - Central Chest Pain > Flashcards

Week 5 - Central Chest Pain Flashcards

1
Q

A 59-year-old male presents in A&E with a crushing chest pain that radiates to the jaw or shoulder for the past 30 minutes. He also feels short of breath and nauseous. O2 is 96% and you carry out an ECG and note that there is ST elevation in leads V3, V4. What part of the heart is likely to be affected by this MI?

A

anterior

V1-4 shows the anterior/septal region of the heart. this typically shows as an infarction in the LAD

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2
Q

what is the way to recall XR findings in heart failure

A

ABCDE

alveolar oedema
Kerley B lines
cardiomegaly
dilation of UPPER lobe vessels
effusions

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3
Q

what is not a chest x-ray finding in chronic heart failure

A

dilation prominent in lower lobe vessels

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4
Q

what is upper lobe venous diversion causes by and what is the clinical name for it

A

Upper lobe venous diversion (cephalisation) is caused by an increase in left atrial pressure (receives from pulmonary system) which can occur in pulmonary oedema.

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5
Q

A 63-year-old man with a history of high blood pressure, presents in A&E with a severe sudden-onset sharp/tearing chest pain, which radiates to the back. From the list below what is your most likely diagnosis?

A

aortic dissection

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6
Q

A 40-year-old woman develops sudden-onset dyspnoea at rest following hip replacement surgery. On examination Her airway is patent, she has a respiratory rate of 28 breaths per minute, oxygen saturation of 90%, bibasal crackles on chest sounds, pulse 132 beats per minute, Heart sounds Normal Sinus Rhythm, bilateral ankle oedema she is alert, blood sugar 6.8, temp 37.8 and abdomen soft non tender. Her electrocardiogram (ECG) shows right axis deviation.

what is the diagnosis

A

Pulmonary Embolism

Patients can also present with signs of hypoxia, pyrexia and later haemoptysis. Look out for risk factors such as recent surgery and immobility in this patient.

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7
Q

A 23-year-old woman presents with localized left-sided chest pain that is exacerbated by coughing and is particularly painful on light pressure to that area. Pain is relieved by aspirin. The ECG is unremarkable. What is the most likely diagnosis?

A

idiopathic costochondritis

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8
Q

what is idiopathic costochondritis also known as

A

Tietze’s Syndrome

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9
Q

what is idiopathic costochondtitis

A

Tietze syndrome is a rare, inflammatory disorder characterized by chest pain and swelling of the cartilage of one or more of the upper ribs (costochondral junction), specifically where the ribs attach to the breastbone (sternum). Onset of pain may be gradual or sudden and may spread to affect the arms and/or shoulders. Tietze syndrome is considered a benign syndrome and, in some cases, may resolve itself without treatment. The exact cause is not known.

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10
Q

what is pericarditis

A

inflammation of the pericardium, the membrane surrounding the heart

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11
Q

what is the potential space between the pericardium and myocardium called

A

the pericardial cavity

the two layers usually touch each other, which is why it is only called a potential space

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12
Q

what are the potential underlying causes of the inflammation

A

Idiopathic (no underlying cause)
Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses)
Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis)
Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma)
Uraemia (raised urea) secondary to renal impairment
Cancer

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13
Q

what medications can cause pericarditis

A

methotraxe

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14
Q

what is pericardial effusion

A

when the potential space in the pericardial cavity fills with fluid. this creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart)

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15
Q

what is pericardial tamponade (cardiac tamponade)

A

where the pericardial effusion is large enough to raise the intra-pericardial pressure

this increased pressure squeezes the heart and affects it’s ability to function

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16
Q

what does cardiac tamponade reduce

A

the heart filling during diastole, decreasing the cardiac output during systole.
this is an emergency and requires prompt draining of the pericardial effusion to relieve the pressure

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17
Q

what are the two key presenting features for pericarditis

A

chest pain
low grade fever

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18
Q

what is the character of the chest pain

A

Sharp
Central/anterior
Worse with inspiration (pleuritic)
Worse on lying down
Better on sitting forward

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19
Q

what is a key examination finding

A

pericardial friction rub on auscultation

a pericardial rub is rubbing, scratching sound that occurs alongside the heart sounds

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20
Q

what would blood tests show in pericarditis

A

raised inflammatory markers (WBC;S, CRP, ESR)

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21
Q

what are the ECG changes seen in pericarditis

A

saddle-shaped ST elevation
PR depression

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22
Q

what can be used to diagnose a pericardial effusion

A

echocardiogram

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23
Q

what is the management of pericarditis

A

Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment (e.g., aspirin or ibuprofen)

Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence)

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24
Q

what are the two most common causes of pericarditis

A

viral infection and secondary to MI

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25
Q

what is Dressler’s syndrome

A

pericarditis that occurs secondary to myocardial or pericardial damage, and occurs at least 2 WEEKS after the MI

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26
Q

what makes Dressler;s different from normal post MI pericarditis

A

at least two weeks after - occurs in 7% of MI patients

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27
Q

what is the pathology behind Dressler’s

A

It is an auto-immune condition whereby the body auto-reacts against damaged myocardial tissue.
Antimyocardial antibodies are often found.

Recurrence is common

May also occur after episodes of unstable angina

Presents with massively raised ESR

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28
Q

where is pericarditis pain often found

A

retrosternal - often radiates to shoulders and neck and is aggravated by deep breathing etc

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29
Q

how is pericardial pain relieved

A

by leaning forwards

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30
Q

what is diagnostic for pericarditis

A

pericardial friction rub

usually heard in systole but may also be heard in diastole

31
Q

what are the dosages of the medications used in pericarditis

A

Colchicine
500mcg BD for 3 months
OD if weight <70kgs

PLUS

Oral NSAID’s
- Ibuprofen 600mg TDS for two weeks, then 200-400mg TDS for 2 weeks, OR
- Aspirin 750-1000mg TDS for 2 weeks and then 250-500mg TDS for 2 weeks
- Do not use NSAID’s in the first few days after MI – as they associated with increased risk of myocardial rupture

32
Q

when is chronic pericarditis said to exist

A

If pericarditis lasts more than 6-12 months, then chronic pericarditis is said to exist. In these cases, it is possible for the pericardium to thicken, and this can restrict ventricular filling, and then restrictive pericarditis is present

33
Q

what is Ewart’s sign

A

this is rare

the effusion can compress the base of the left lung producing an area that is dull to percussion, just below the angle of the left scapula

34
Q

what is constrictive pericarditis usually a result of and what happens to the pericardium

A

can be a result of TB and other infectious causes

the pericardium may become hard, fibrous and calcified.

it also occurs after open heart surgery

35
Q

when do we say constrictive pericarditis is present

A

if it starts to interfere with ventricular filing

36
Q

what is constrictive pericarditis very difficult to distinguish from and what is used to diagnose

A

Constrictive pericarditis is very difficult to distinguish from restrictive cardiomyopathy. The final diagnosis may depend on complex Doppler flow studies.

37
Q

what is the treatment for constrictive pericarditis

A

complecte resection of the pericardium

this is dangerous and has a high rate of complications

38
Q

what is myocarditis

A

inflammation of the myocardial layer of the heart muscle

39
Q

what is the myocardium responsible for

A

it is the middle layer composed of cardiac muscle that is responsible for the heart contraction

40
Q

what can the inflammation lead to

A

damaged myocardial cells, weakening of the heart’s pumping capacity and if severe, it can lead to acute-onset heart failure

41
Q

what is acute onset heart failure secondary to myocarditis called

A

fulminant myocarditis

42
Q

what is the epidemiology of myocarditis

A

All age groups can be affectedbut it commonly affects those <50
Slightly higher incidence in men than women
5% of patients with acute viral illness may have myocardial involvement
Approximately 10% of all sudden cardiac deaths in people under 35 can be attributable to myocarditis aetiology

43
Q

what are the infectious causes of myocarditis

A

Viral (main cause);
Coxsackie viruses are the commonest culprits in Europe and North America

Other common causes:
Adenovirus
Influenza A and B
HIV
EBV
Hep B and C
Diphtheria (commonest cause globally)
There are also (less common) bacterial and fungal causes

44
Q

which drugs may cause myocarditis

A

Cyclophosphamide, catecholamines (e.g. adrenaline, dopamine)

Amphetamines, ethanol, cocaine

Heavy metals (copper, iron, lead)

45
Q

what is the typical presentation of myocarditis

A

can be variable - from asymptomatic all the way to life threatening heart failure

it is important to consider in a differential of chest pain, only about 1/3 of patients will present with chest pain, and over half will have fatigue

46
Q

what are the symptoms of myocarditis

A

Fatigue
Chest pain (can be positional)
Dyspnoea/orthopnoea
Palpitations, syncope

47
Q

what is sound on examination for myocarditis

A

S3 and S4 gallops
Pericardial rub
Tachycardia (arrythmias)

48
Q

what will an ECG show for myocarditis

A

ST depression or elevation
T wave inversion
AV node block

49
Q

what would the blood results be in myocarditis

A

raised troponin and CK-MB

50
Q

if there is left ventricular dysfunction what treatments are given

A

ACEi/ARB

51
Q

what is the prognosis for myocarditis

A

Although prognosis for many patients is good, where they have little or no residual loss of cardiac function, for some types of myocarditis (e.g. giant cell myocarditis), the prognosis can be very poor and result in death at <6 months post symptom onset.

52
Q

what is stable angina a common presentation of

A

CDH

53
Q

what is angina

A

myocardial ischaemia without infarct

54
Q

how does angina typically present

A

Angina typically presents as central or left sided chest pain, with or without radiation to the neck, arm or jaw, and is generally transient, most commonly occurring on exertion, but can also be triggered by emotion

55
Q

what are acute angina attacks usually treated with

A

nitrates

56
Q

what does long term management of angina include

A

Long-term management involves the use of beta-blockers, calcium-channel blockers, long-acting nitrates, aspirin and statins

57
Q

what is the typical presentation of stable angina

A

Central or left sided chest discomfort
May radiate to the jaw, arm epigastrium – like ACS pain
Can vary from mild to severe
Usually described as a “tight” or “crushing” sensation
Dyspnoea may or may not be present
Usually results from exertion
Symptoms relieved by rest
Symptoms typically of several minutes duration – shorter acting symptoms of a few seconds only are unlikely to be ischaemia related
Patient may get frequent symptoms (several times daily) or only rarely (months between episodes)
This does not necessarily correspond to the severity of the disease

58
Q

what is crescendo angina

A

when attacks are increasing in frequency and/or severity and is correlated to high risk of severe ACS

59
Q

when do you treat chest pain as ACS and not angina

A

if the pain doesn’t resolve within 5 minutes of cessation of active, and/or with use of GTN spray, treat as ACS

60
Q

what are the typical causes of angina

A

atheroma
aortic valve disease
hypertrophic cardiomyopathy

61
Q

what can the changes in ECG be in stable angina

A

pathological Q waves
ST depression
LBBB
T wave flattening or inversion

62
Q

what is the usual first line investigation for stable angina and according to NICE, the primary diagnostic investigation

A

usually CT coronary angiogram (CTCA)

63
Q

where can the pain for stable angina usually be felt

A

behind the sternum

64
Q

what artery narrowing is associated with a poor prognosis

A

left main coronary artery or left anterior descending artery

65
Q

what is the Canadian Cardiovascular Society Angina Classification

A

Class I – ‘Ordinary Activity’ (e.g. walking or climbing stairs) does not precipitate angina

Class II – Angina precipitated by walking upstairs, cold weather, or meals

Class III – marked limitation of normal physical activity

Class IV – Symptoms present at rest, unable to carry out many normal physical activities

66
Q

what are the two main mechanisms used to relieve the symptoms of angina

A

increasing blood flow to the heart muscle by dilating the coronary arteries with GTN

decreasing the workload on the heart

67
Q

what are the first line treatments to decrease the workload on the heart

A

beta blockers

calcium channel blockers

68
Q

what are examples of beta blockers and what do they do

A

(e.g. atenolol or metoprolol)

Proven to reduce MI and sudden death risk
Decreases heart rate, contractility, and cardiac output – which reduces cardiac O2 demand
e.g. metoprolol 25mg BD

69
Q

give examples of CCB and what do these do

A

Calcium channel blocker (e.g. verapamil, diltiazem)

These two agents are preferred due to their negative chronotropic events
Typically reserved for patients who are unable to tolerate beta-blockers or whose symptoms are incompletely controlled with beta-blockers

70
Q

what are the second line treatments for stable angina

A

Long acting nitrate
e.g. isosorbide mononitritae 30mg PO OD – up to a max of 120mg daily
Typically effect lasts for 4-6 hours
Nicorandil
Ivabradine
Ranolazine

71
Q

what are third line treatments

A

PCI
CABG

72
Q

what is the investigation of choice for a child with suspected heart disease

A

echocardiography

73
Q
A

Year 3 (63 decks)

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