Case 5: Central Chest Pain Flashcards
How can coronary artery occlusion lead to heart failure?
- blockage of coronary artery
- ischaemia and MI
- necrosis
- inflammatory response to remove dead cells
- infarct healing and scar formation
- hypertrophy, dilation and reduced function
- heart failure
describe the chest pain in a pneumothorax
sudden onset pleuritic chest pain either left sided or right sided with associated dyspnoea and syncope
describe the chest pain in MSK
pain is normally persistent and is worsened with passive and active motion and sometimes chest tenderness on palpation
describe the chest pain in stable angina
exertional pain or discomfort in the centre of left side of chest, throat, neck or jaw - it is relieved by rest or GTN within a few minutes. it may radiate to the neck/jaw/left arm. there also may be breathlessness
describe the chest pain in pericarditis
constant or intermittent central pleuritic harp pain which is often aggravated by position (worse on lying down and relieved by sitting or leaning forward)
describe the chest pain in peptic ulcer disease
recurrent and vague epigastric discomfort which is relieved by food or antiacids
describe the chest pain in PE
sudden onset pleuritic chest pain with associated dyspnoea and tachycardia. sometimes mild fever, haemoptysis and syncope
what are the cardiac causes of central chest pain?
acute coronary syndrome
stable angina
thoracic aorta dissection
myocarditis
pericarditis
describe the chest pain in thoracic aorta dissection
Sudden, tearing pain radiating to the back
what are the respiratory causes of chest pain?
pulmonary embolism
tenion pneumothorax
pneumonia
pleurisy
what are the GI causes of chest pain?
oesophageal rupture
peptic ulcer disease
pancreatitis
gallstones
hepatitis
GERD
what is the pathophysiology of stable angina?
atherosclerosis and atheroma formation results in progressive narrowing of the lumen in a coronary artery
at rest there is no chest pain but during exertion the myocardial demand rises and the supply cannot meet the myocardial demand resulting in an exertional chest pain that is relieved by rest or GTN
what is the pathophysiology of ACS?
an unstable plaque can rupture resulting in platelet aggregation and thrombus formation which can cause sudden occlusion of the coronary artery. this results in acute chest pain called ACS
the degree and duration of the occlusion will dictate the subtype of ACS
- total and persistent occlusion = STEMI
- partial or temporary occluion = NSTEMI or unstable angina
what is the pathway for a patient coming to hospital with chest pain?
all patient with acute chest pain (lasting more than 15 minutes) will need an immediate 12 lead ECG to exclude ST elevation. if there is no ST elevation then the patient will need to undergo 6 hour troponin testing
if troponin is elevated = NSTEMI
and if not = unstable angina
what are the 3 main diagnostic features of angina?
- constricting discomfort in the front of chest, neck, shoulders and arms
- precipitated by physical exertion
- relieved by GTN or rest in about 5 minutes
what are the sub types of angina?
they depend on how many of the typical diagnostic features are present:
3 - typical angina
2 - atypical angina
1/0 - non angina
what are the main risk factors for angina?
smoking
hypertension
hyperlipidaemia
low LDL
diabetes
male
obesity
family history
ilicit drug use
what investigations do you carry out for someone with suspected angina?
- detailed chest pain history (SOCRATES)
- cardiovascular examination
- BP/BMI
- 12 lead ECG
- routine bloods: FBC, renal function, glucose, troponins (to rule out ACS)
diagnostic tests:
1. CT coronary angiogram (gold standard)
2. stress ECHO, MRI regional wall, SPECT
what ECG changes can be seen in stable angina?
pathological Q waves
LBBB
ST segment changes
T wave changes
all indicative of CAD
what is the RAMP management of stable angina?
R - refer to cardiology
A - advise of diagnosis and self management
M - medication treatment
P - procedural/surgical intervention
what is the medical management of stable angina? contradindications?
FOR IMMEDIATE SYMPTOMATIC RELIEF:
- GTN spray is used as required in acute attacks. take and repeat after 5 minutes is required
FOR LONG TERM SYMPTOMATIC RELIEF:
- beta blocker (bisoprolol)
- calcium channel blocker (amlodipine)
CONTRAINDICATIONS:
As monotherapy, a rate-limiting calcium channel blocker should be used such as verapamil
When in combination with a beta blocker, a long acting calcium channel blocker should be used, e.g. modified release nifedipine
Verapamil should not be used with a beta blocker if there is a risk of complete heart block.
what medications do we give for secondary prevention of stable angina?
4 A’S:
Aspirin
Atorvostatin
ACE inhibitor
Already on beta blocker for symptomatic relief
what is the general lifestyle advice given to someone with stable angina?
smoking cessation
glycaemic control
hypertension control
hyperlipidaemia control
weight loss
reduce alcohol intake
what are the surgical interventions for stable angina?
PCI:
percutaneous coronary intervention
this involves putting a catheter into the patient’s brachial or femoral artery and feeding it up into the coronary artery and injecting a contrast so that any areas of stenosis are highlighted on xray and then this can be treated with balloon dilatation and insertion of a stent
CABG:
opening the chest along the sternum and taking a graft vein from the patients leg and sewing it onto the affected coronary artery to bypass the stenosis.
what are the three types of acute coronary syndrome?
unstable angina - this is angina that occurs at rest for extended periods of time or a new onset severely increased form of stable angina. no sign of myocardial ischaemia
NSTEMI - caused bys evre/incomplete stenosis of a coronary artery. MI presenting complaints with evidence of biochemical myocardial ischaemia and some ECG changes
STEMI - complete compromise to coronary perfusion presenting as an MI with definitive ECG changes and evidence of biochemical MI
what is the typical pain of ACS?
S - central/left sided pain
O - sudden onset
C - crushing (weight on chest)
R - left arm, neck and jaw
A - nausea, vomiting, sweating, SOB, syncope
T - constant
E - stress and exertion worse, GTN may help
S - often unbearably extreme
what is the typical presentation of someone with ACS?
central and constricting chest pain associated with:
nausea
vomiting
sweating
SOB
palpitations
pain radiating to the arm/jaw
what are the risk factors for ACS?smoking
hypertension
lDL
obesity
diabetes
stress
diet
physical inactivity
age
male
family history
BAME
what investigations do you carry out for someone with suspected ACS?
physical examination
bloods
ECG (most important)
CXR
CT angiogram
echocardiogram
how do you diagnose unstable angina?
cardiac chest pain + abnormal/normal ECG + normal troponin (after serial repeats)
how do you diagnose NSTEMI?
cardiac chest pain + abnormal/normal ECG (no ST elevation) + raised troponin
how do you diagnose STEMI?
cardiac chest pain + persistent ST elevation/new LBBB
how do you differentiate between a NSTEMI and stable angina?
We differentiate between a NSTEMI and unstable angina by performing a blood test. Raised troponin and/or other ECG changes (ST depression/T wave inversion/pathological Q waves) then diagnosis is NSTEMI. Normal troponin and ECG with no pathological changes = unstable angina, or another cause e.g. MSK chest pain
what ECG changes can be seen in a STEMI/NSTEMI?
NSTEMI
-ST segment depression in a region
- Deep T wave inversion/flattening
- Pathological Q waves
STEMI
- ST segment elevation >1mm in adjacent limb leads (I, II, III, aVF, aVL)
à ST segment elevation >2mm in adjacent chest leads (V1-V6)
à New left bundle branch block with chest pain or suspicion of MI
is tropnonin a good investigation?
it is a cardiac regulatory protein that controls the interaction between myosin and calcium and is released in cardiac damage
it is not specific as it is also raised by:
- pericarditis
- myocarditis
- arrhythmias
- defibrilation
- acute heart failure
- PE
- type A aortic dissection
- prolonged exercise
what is the acute treatment of ACS?
MONA
M - Morphine
O - oxygen if saturation is less than 94%
N - nitrates
A - aspirin
C - clopidogrel or ticagrelor
what is the acute treatment of a STEMI?
if someone presents with a STEMI, within 12 hours of onset of symptoms:
1. primary PCI (if available within 2 hours of presentation)
2. thrombolysis (if PCI is not available within 2 hours)
PCI discussed earlier
thrombolysis involves inhecting a fibrinolytic medication to rapidly dissolve clots but does pose a risk of bleeding
what fibrinolytics are used in thrombolysis?
streptokinase
alteplase
tenectoplase
what is the acute treatment of a NSTEMI?
BATMAN
B - beta blockers
A - aspirin
T - ticagrelor or clopidogrel
M - morphine
A - anticoagulant (LMWH) N - nitrates
what is a GRACE score?
this is the scoring system used to assess the need for PCI in a STEMI. it gives a 6 month risk of death or repeat MI after having a NSTEMI
<5% low risk
5-10% medium risk
>10% high risk
what is the secondary prevention of ACS?
6 A’s
A - aspirin
A - antiplatelet (ticagrelor or clopidogrel)
A - atorvostatin
A - ace inhibitor (ramipril)
A - atenolol (beta blocker)
A - aldosterone antagonist (eplerenone)
what are the types of MI?
type 1 = traditional MI due to acute coronary event
Type 2 = ischaemia secondary to increased oxygen demand or reduced supply of oxygen (e.g. severe anaemia, tachycardia or hypotension)
type 3 = sudden cardiac death or cardiac arrest suggestive of an ischaemic event
type 4 = MI associated with procedures such as PCI or coronary stenting
what is dressler’s syndrome?
Post MI (2-3 weeks) localised immune response - delayed pericarditis
Presents with pleuritic chest pain, low grade fever, pericardial rub on auscultation
Diagnosis:
- ECG global ST elevation and T wave inversion
- Echo - pericardial effusion
- Raised inflammatory markers - CRP and ESR
Management is with NSAIDS (aspirin/ibuprofen) and in more severe cases with steroids such as prednisolone. May need pericardiocentesis to remove the fluid from around the heart.
what is the pathophysiology of aortic dissection?
it is a rare but serious cause of chest pain. it occurs when there is a tear in the intima of the wall of the aorta. high pressure blood in the aorta then begins to tunnel between the intima and media which separetes the 2 layers. as more of the tunica intima is shed from the tunica media blood starts to pool between the 2 layers and becomes a bulge
what are the risk factors for aortic dissection?
chronic hypertension
trauma
bicuspid aortic valve
marfans syndrome
turners and noonan’s syndrome
pregnancy
syphillys
what are the symptoms of an aortic dissection?
chest pain radiating to the back. typically a severe and harp pain tearing in nature which is maximal at onset
pulse deficit - weak or absent pulse OR variation (>20mmHg) in systolic BP between the arms
pulsus paradoxus
muffled heart sounds
distended neck veins
aortic regurgittaion
hypertension
what is pulsus paradoxus?
moderate to severe cardiac tamponade, and occasionally constrictive pericarditis, induce haemodynamic changes that enhance the inspiratory fall in systolic BP (>10mmHg). this exaggerated drop in systemic BP during inspiration is termed pulsus paradoxus.
what are the two classifications of aortic dissection?
type A - ascending aorta. 2/3 of cases, more typically chest pain
type B - descending aorta distal to left subclavian. 1/3 of cases, more typically back pain
what are the complications of aortic dissection?
- Blood can flow back up the aorta to the heart and fill the pericardial space leading to cardiac tamponade.
- Blood flowing through the false lumen can also puncture a hole through the tunica media and externa. Blood can then flow into the mediastinum.
- Blood could continue to flow between the 2 layers until it reaches another artery that branches off the aorta e.g. renal/subclavian. Blood in the false lumen can put pressure on these branches arteries, decreasing blood flow to the area respectively
what investigations are carried out for aortic dissection?
CT angiography of the chest abdomen and pelvis is the investigation of choice. It is suitable for stable patients and for planning surgery. The main diagnostic finding is a false lumen.
For more unstable patients a transoesophageal echocardiography is more suitable.
what is the treatment of an aortic dissection?
Aortic dissection needs to be treated immediately
Type A
Treated surgically. Dissected aorta is removed. This blocks the entry of blood into the wall of the aorta. Wall is then reconstructed with synthetic graft
Type B
Conservative management. Treated with beta blocker and nitroprusside and bed rest.
