Central chest pain (Chronic) Flashcards
1
Q
What are the differentials for chest pain (both acute and chronic)
A
- Split into 4 potential regions 1) cardiac causes 2) respiratory causes 3) upper GI causes 4) MSK/other
1 cardiac:
- ACS
- Angina pectoris
- Pericarditis
- Cardiac tamponade
- aortic dissection
2: Resp:
- PE
- Pneumothorax
- Pneumonia
- Pleurisy
- Lung malignanct
3: Gastro:
- GORD
- peptic ulcer disease
- oesophageal spasm
- acute cholecystitis
- pancreatitis
- gastritis
4: MSK/ other:
- Costochondritis
- Trauma - -> recent rib fracture?
- Anxiety or panic attacks?
- Shingles or herpes zoster?
2
Q
What are the common causes of chronic central chest pain:
Differentials listing in LO’s?
A
- Cardiac —> angina pectoris
- Upper GI –> GORD
- Psychological –> anxiety or panic attacks
- MSK –> Costochondritis/ trauma/ shingles (herpes zoster)
3
Q
LO: Take a focused history on chest pain to identify key features (including risk factors) and use these to formulate appropriate differential diagnoses
A
-
SQITAS -
- site –> radiation to jaw/ down the left arm (ACS or stable angina)
- quality of the pain –> sharp/ dull/ acheing? (how would they describe it, does it come and go?) Burning (think GORD)
- intensity
- timing - first onset, how long does the pain last, have they had the pain before?
- alleviating factors - e.g. better with rest/ with GTN spray (Oeosphageal spasm or ACS)/ sitting forward (think pericarditis)
- worsening factors –>worse after eating or taking a deep breath in (think pleuritic pain e.g. pneumonia or pneumothorax/PE), worse on lying flat (GORD)
- associated symptoms –> sweaty/clammy/ SOB (Think ACS or angina) cough/ palpitations/ LOC? Fever and fatigue (pericarditis). Dysphagia/ heartburn or regurgitation (GORD or oesophageal spasm).
- PMH –>
- surgery –> CABG/ coronary artery stents or heart valve replacements
- CV risk factors–> HTN/ hyperlipidaemia/previous MI/ diabetes
- cvd –> OTHER –> angina/ obesity / CKD/ AF/ stroke/PVD/ rheumatic fever?
- Resp disease –> pneumonia/ pneumothorax/ pe
- GI disease –> GORD or oesophageal spasm
- Drug Hx: anticoagulants/ antiplatets/ statin/ GTN/ CCB/ Ace i / Abx/ colchicine (pericarditis)
- Family hx –> CVD
- SH:
- smoking (CV risk factor)
- Alcohol
- Recreational drugs –> cocaine/ ectasy/ amphetamines can activate SNS –> tachycardia (palpitations), BP abnormalities, coronary artery vasospams (chest pain).
- Occupation –> sedentary?
- general lifestyle –> exercise and diet
4
Q
Key features for differentials of chest pain in history?
ACS
Stable angina
Pericarditis
Thoracic aortic dissection
pneumonia
spont pneumothorax
PE
GORD
Oesophageal spasm
A
- ACS –> sudden onset central crushing chest pain, radiation to left arm and or jaw and lasting longer than 20 mins. Sweatiness, clamminess, nausea and SOB. Worse on exertion, better with GTN.
- Stable angina –> sudden onset central chest pain radiating to left arm/ jaw, lasts fewer than 20 mins, complete resolution at rest. Triggered by exertion, resolves with GTN spray or rest. SOB associated.
- pericarditis –> gradual onset chest pain, worse on lying flat, better leaning forwards, associated with fever and fatigue
- Thoracic aortic dissection –> sudden onset central chest pain, radiating through to the back and often “tearing” in nature. Associated with presyncope and syncope secondary to haemodynamic instability.
- Pneumonia –> gradual onset sharp chest pain worsened by deep insipiration (pleuritic in nature). Associated sx include productive cough/ SOB/ fever and malaise
- Spontaneous pneumothorax –> sudden onset sharp chest pain, worse on inspiration, SOB
- PE –> sudden onset chest pain worse in inspiration, SOB and haemoptysis
- GORD –> gradual onset chest pain , typically burning in nature , worsened lying flat, assocaited with nausea and vomiting
- oesophageal spasm –> sudden onset central chest pain relieved by GTN spray (hence confused with ACS), associated with dysphagia, heartburn and regurgitation.
5
Q
Chest pain: general investigations?
A
6
Q
Differentials:
Angina pectoris
define
two types
Pathophysiology - of ischaemia and pain?
A
- Angina pectoris = chest pain due to inadequate supply of oxygen to the heart muscle - transient myocardial ischaemia but without infarction. Typically precipitated by exertion or psychological stress, relieved by rest or sublingual nitrogen.
- Divided into stable angina and unstable angina (part of ACS)
- Stable –> relationship between workload/ demand and ischaemia is predictable. Most common, 70% artery stenosis blocked by plaque build up. Enough to supply heart at rest, under stress heart worload increases, blood flow cannot meet metabolic demands –> ischaemia and pain.
- Unstable –> clinically worsening angina, angina at rest or with increasing frequency/ intensity of episodes.
-
Pathophysiology: of ischaemia
- Narrowing of the coronary arteries supplying the heart muscle due to atherosclerosis
- In stable angina –> 70% Coronary artery stenosis
- In unstable angina –> often caused by rupture of atherosclerotic plaque in CA –> leading to thrombosis or blood clot to develop on the plaque. Occlusion doesnt block entire vessel but heart becomes starved of oxygen –> subendocardial ischaemia –> can develop into MI (where heart muscle has already become necrotic.)
- Hypertrophic cardiomyopathy –> greater volume of cardiac muscles which requires more oxygen deliver –> angina
- pumping against high pressure (aortic stenosis or HTN)
- coronary artery vasospasm (Prinzmetal angina)–> random vasoconstriction of the CA’s, serious and transmural ischaemia
- Narrowing of the coronary arteries supplying the heart muscle due to atherosclerosis
-
Pathophysiology: of ischaemia pain
- Coronary arteries lie on top of epicardium, then dive down into the myocardium to supply it and the endocardium.
- With reduced BF, less oxygen is delivered to the subendocardium leading to ischaemia
- leads to release of adenosine and bradykinin –> pain
7
Q
Angina pectoris: history features
A
- Typical presentation:
- pain –> pressure/ squeezing/ heavy
- radiation to left arm, jaw, shoulders or back
- SOB
- diaphoresis
- Symptoms last less than 20 mins
- subside after exertion or stress removed
- If unstable –> pain during exercise or stress or at rest, lasts > 20 mins
- relived with rest or GTN
- Other sx/ less common = fatuge/ nausea/ indigestion/ light headedness (more common in women).
8
Q
Angina pectoris : examination features
A
- BMI, BP and vitals
- pulse rate and ryhtm
- heart murmurs
- nicotine stains
- xanthelasmata –> hypercholesterolaemia
- raised JVP/ ankle oedema/ crackles on ausc
- signs of atherosclerotic disease —> diminished pedal pulses carotid bruit
- fundoscopy –> increase light reflex and arteriovenous nicking (HTN)
9
Q
Angina pectoris: Investigations
A
- Resting ECG –> may show non specific ST depression - indicates ischaemia or Q waves (indicates a prior infarction).
- Bloods:
- Hb –> anaemia results in additional cardiac workload and reduced O2 delivery to the heart, can exacerbate angina
- U & E - prior to ACE i and other HTN medications, check kindey function (CKD RF for CAD)
- LFT’s - prior to starting statin and also for clotting/ coagulability
- lipid profile –> dyslipidaemia v important RF for IHD –> elevated LDL cholesterol = increased risk, elevated HDL = protective
- fasting blood glucose or HbA1c –> DBM = RF IHD
- TSH –> hyperthyroidism can increase CO and workload, exacerbating angina
- Imaging:
- CXR
- rest echocardiography –> often normal, may reveal focal wall abnormalities from prior infarction
- exercise ECG (before, during and after exercise, HR achieved and haemodynamic response) – >ST segment elevation and depression = ischaemia
- cardiac CT angiography or invasive angiography – >narrowing > 50%
10
Q
Angina pectoris: management?
A
-
Conservative:
- Lifestyle modifications –> Exercise, diet (reduced trans fatty acids and saturated fats), weight loss, smoking cessation, stress management
-
Medical:
-
Antiplatelet therapy --> protect against platelet activation and acute thrombosis (reduced risk MI)
- Low dose aspirin
- Clopidogrel if aspirin intolerant
- If ACS episode dual therapy for a year
-
Beta blockers
- decrease heart rate and Myocardial contractility, therefore reduced myocardial oxygen demand
-
RAAS Antagonists
- In patients with HTN/ DM/ LVEF/CKD –> ACEi to reduce ATii and increase bradykinin –> reduced LV and vascular hypertrophy, atherosclerosis progression, plaque rupture and thrombosis.
-
Lipid management
- Statin therapy = mainstay of therapy –> reduced major coronary events –> reduce LDL (reduce atherosclerotic progression).
-
BP control
- lifestyle often adequate –> exercise, low salt diet, weight reduction, moderate aclochol
- Treat > 140/ 90 mmHg
-
Diabetes management
- Glycaemic control to reduce risk of macrovascular complications of angina/MI / revascularisation
-
Anti- angina to reduce symptoms:
- Sublingual GTN - for immediate relief short term
- BB are first line therapy (reduce cardiac demand)
- can add CCB (verapamil or diltiazem with caution when with BB) or long acting nitrate
-
Antiplatelet therapy --> protect against platelet activation and acute thrombosis (reduced risk MI)
- Surgical: coronary revascularisation –> either by CABG or PCI –> for patients with symptoms despite maximal medical therapy.
- PCI –> catheter, coronary angioplasty and stent (drug eluting) into the coronary artery, done if proximal or extensive disease in the coronary arteries
- CABG -> for patients with severe stenosis. midline sternotomy incision and graft from great saphenous vein sewed onto affected coronary artery to bypass the stenosis. Recovery slower and complications higher than PCI.
11
Q
Differential diagnoses chronic chest pain: GORD
Define
Pathophysiology
A
- GORD = symptoms of complications resulting from the reflux of gastric contents into the oesophagus and beyond, into the oral cavity or lung
Pathophysiology:
- The low oesophageal sphincter regulates food passage from the oesophagus to the stomach - contains both intrinsic smooth muscle and skeletal muscle
-
Anatomy of LOS:
- Physiological sphincter located at Gastrooesophageal junction - situated at the left of T11 vertebra, marked by squamocolumnar junction (squamous mucosa of oesophagus and columnar mucosa of stomach meet).
- LOS due to:
- oeosphagus entering stomach at acute angle
- folds of mucosa help occlude lumen
- right crus of diaphragm insertion
- Episodes of transiet LOS relaxation occur more frequently in GORD - causes reflux of gastric contents into the oesophagus
- Can also have permanent LES relaxation, or transient increase of intraabdominal pressure that overcomes LES pressure
- Delayed gastric emptying –> may increase intragastric pressure
- More likely to have reflux with hiatus hernia, leads to decrease resting lower oesophageal sphincter pressure.
- severity of mucosal damage depends on duration of contact with gastric contents (acid, pepsin, and bile salts all damage the mucosa)–> depends on no of episodes, efficacy of oesophageal peristalsis and neutralisation of acid by saliva
- Can lead to Barrett’s oesophagus –> metaplasia (reversible change from one differentiated cell type to another) of LE squamous epithelium to gastric columnar epithelium.
12
Q
GORD: history
Risk factors
presenting symptoms - common and uncommon
RF’s in GORD hx?
A
- Risk factors: obesity, older age, hiatus hernia, family hx of heartburn or GORD
- Presenting sx:
- burning chest pain typically after meals
- typically retrosternal
- Can be worse on lying down or bending over
- relieved by antacids
- reflux of acid into the mouth with sour or bitter taste
- water brash - excessive saliva production to counteract stomach acid
- dysphagia (feeling food is stuck)
- bloating and early satiety
- globus –> patients describe lump in the throat
- dyspepsia/ indigestion (bloating/ nausea/ burping)
- halitosis
- enamel erosion
- atypical –> laryngitis/ hoarse voice from vocal cord irritation, coughing/ wheezing from aspiration gastric contents into tracheobronchial tree.
- Red flags:
- Anaemia, dysphagia, haematemesis, melaena, persistent vomiting or involuntary weight loss - oesophagitis, peptic stricture, cancer
13
Q
Red flag features that indicate need for 2 week referral for endoscopy?
A
- aged over 55 years
- dysphagia *at any age
- unintentional weight loss
- anaemia - low Hb
- high platelets
- treatment resistant dyspepsia
14
Q
GORD: Investigations
A
- Diagnosis of GORD is usually clinical and supporting by testing when required
- Plus bloods –> FBC for aneamia
- H. pylori testing –> urease breath test or stool antigen test. A CLO test –> done at the time of OGD, biopsy of gastric mucosa is taken. CLO= campylobacter like organism –> rapid urease test for h pylori infection, detects urease secreted from bacteria, catalyses conversion of urea to ammonia and CO2. Performed at the time of gastroscopy, take biopsy of mucosa from antrum of stomach and place in medium.
- If typical sx –> short trial 8 weeks of PPI and lifestyle therapy (weight loss and elevation of head of bed for nocturnal). Symptom relief is diagnostic, failure of PPI does not exclude GORD.
- Longstanding, unresponsive or atypical sx –> Upper endoscopy (oesophagogastroduodenoscopy)
- May identify oesophageal malignancy, peptic ulcer or barrets oesophagus
- PPI therapy withheld prior to endoscopy to assess whether there is excessive oesophageal acid exposure
- Alarm signs: weight loss, dyshagia, odynophagia (painful swallowing) or malaena. –> Endoscopy
- Can do barium swallow in patients where endoscopy is contraindicated/ unavailable
- manometry after endoscopy –> evaluates oesophageal contractions and LES function
- ambulatory pH or impedance pH testing done if manometry is normal –> identifies patients whose sx correlate with oesophageal acid
15
Q
GORD: management
A
- Conservative:
- Lifestyle –> weight loss, smoking cessation, head of bed elevation, avoidance of late night eating and smaller lighter meals, routine food eliminations (caffiene, alcohol)
- Medical:
- patients < 40 yrs w typical sx and no RF’s – > start standard dose PPI ~ 8 weeks - start lowest effective dose PPI
- if inadequate response - high dose PPI and endoscopy
- If endoscopy fails to show erosive oesophagitis or barrett’s –> refer gastroenterologist
- Red flags or > 40 yrs or atypical sx –> endoscopy
- OTC - gaviscon (sodium alginate, sodium bicarb, calcium bicarb) and rennie (calcium carbonate, magnesium carbonate)
- Alternative to PPI - H2 antagonists - ranitidine, cimetidine
- Surgical:
- antireflux surgery –>laproscopic fundoplication - tie fundus of stomach around the Lower oesophagus- for individuals responsive to PPI but cannot be on longterm
- bariatric surgery for obese patients with GORD
17
Q
What are the ALARM symptoms for GORD?
A
