Acute Central Chest Pain

Question 1

What are the common causes of acute central chest pain?

Answer 1

Chest pain either benign or serious, cardiac or non cardiac causes:

Common:

ACS - unstable angina, NSTEMI, STEMI

Stable Angina (ANGINA PECTORIS)

acute pericarditis (inflammation of pericardium)

Pneumonia

Viral pleuritis

Costochondritis

GORD

Anxiety or panic disorder

Question 2

What are the less common causes of acute central chest pain?

Answer 2

• Lungs:
  
  • PE
  • Pneumothorax
  • Pulmonary hypertension
• Heart:
  
  • Pericarditis
  • cardiac tamponade
  • mitral valve prolapse
• Aortic –> dissection or prolapse
• GI:
  
  • peptic ulcer
  • oesophageal spasm
  • acute pancreatitis
  • acute cholecystitis
  • gastritis
• Viral:
  
  • herpes zoster

Question 3

Demographics and risk factors for ACS?

Answer 3

• Smoking
• Age –> men > 45 yrs, women > 55 yrs
• family history of coronary artery disease
• male sex
• hypertension
• hyperlipidaemia
• diabetes
• stroke
• peripheral arterial disease
• inactivity and obesity
• illicit drug use
• Be aware in women and older people > 75 yrs, or diabetics they may present with atypical sx such as nausea or dysponea.

Question 4

What are the risk factors for pericarditis?

Answer 4

• More common in adults 20- 50 yrs
• more common in men
• Post MI - early due to local inflammation at epicardial border, later (1 wk - months = Dressler’s syndrome)
• Autoimmune disease- rheumatoid arthritis or lupus
• bacterial/ fungal/ viral infection - viral most common
• trauma or injury
• kidney failure - uraemic pericarditis or dialysis associated pericarditis

Question 5

Risk factors for pneumonia?

Answer 5

• Children < 2 yrs
• adults > 65 yrs
• hospitalisation
• chronic disease - e.g. asthma, copd, heart disease
• smoking
• weakened immune sx –> chemo/radiotherapy, organ transplant, long term steroids, HIV/AIDS

Question 6

viral pleuritis RF

Answer 6

Cocksackie B viral infection

Question 7

Risk factors for costochondritis

Answer 7

• microtrauma - recent history of coughing or unaccostomed repetitive upper limb movement
• women
• over 40 yrs
• hispanic

Question 8

RF for GORD

Answer 8

• Fam hx of heartburn/ GORD
• older age
• hiatus hernia
• obesity
• LOS tone reducing drugs –> calcium channel blockers, alpha/beta adrenergic agonists, thephylline, anticholinergics
• stress
• NSAIDS
• smoking
• alcohol
• asthma

Question 9

RF for generalised anxiety

Answer 9

• Fam hx
• Physical/ emotional stress
• hx of physical/ sexual/ emotional trauma
• other mental health disorders - particularly panic disorder, social phobia, specific phobia
• chronic health condition
• female

Question 10

Focused history of acute central chest pain:

Answer 10

SOCRATES

• Site –> central chest?
• Onset –> duration of pain (differentiate between stable angina vs acute coronary syndrome), did it happen suddenly or build gradually? what were they doing at the time? (Exertion vs rest)
• Character –> Aching or crushing = ACS
  
  • Sharp pain worse on inspiration = pleuritic –> think PE/ Pneumothorax
• Radiation
  
  • left arm and jaw –> typical of ACS
  • radiation through to the back –> aortic dissection
• Associated symptoms:
  
  • Dysponea –> exertiona// orthopnea/ paroxysmal nocturnal dysponea
  • sweating/ claminess/ nausea –> ACS
  • cough? –> duration, sputum (Pneumonia), haemopytsis (PE)
  • palpitations? –> tap out rhythm
  • syncope/ dizzy –> postural/ exertional/ random
  • oedema –> peripheral oedema (lower limbs)
  • fever –> pericarditis/ costochondritis/ pneumonia
• Time –> duration (min/ hrs/ days/ wks) and is it worsening/ fluctuating?
• Exacerbating / relieving factors?
  
  • inspiration worsens pain = PE/pneumothorax/pneumonia
  • Exertion = ACS/PE/Pneumothorax/pneumonia
  • Lying flat = pericarditis, better leaning forward
  • GTN spray betters = ACS or oesophageal spasm
• Severity –> 0-10 scale

Systems review:

CV - chest pain/ palpitations/ dysponea/ syncope / orthopnea / peripheral oedema

Respiratory - dysponea / cough/ sputum/ wheeze/ haemoptysis

GI - nausea/ vomiting/ indigestion/ dysphagia/ weight loss/ abdo pain / bowel habit

CNS - headache/ vision/ motor or sensory disturbance/ loss of conciousness

PMH –>

• Heart:
  
  • Angina/ MI/ grafts or stents
  • HTN
  • Hyperlipidaemia
  • Aortic aneurysm/ dissection
• Respiratory -> pneumonia/ pneumothorax/PE
• GI disease –> GORD/ oeosphageal spasm

Drug hx:

• Antiplatelets or anticoagulants
• GTN
• contraceptive pill –> increased risk thromboembolic disease
• OTC/ allergies

Social hx:

• ​Smoking
• alcohol
• recreational drugs - cocaine and coronary artery vasospasm
• diet - obesity/ fat/ salt intake
• exercise
• Living situation/ ADL

ICE

Question 11

Differentials: Signs and symptoms

How can pain present differently?

what pain presentations are typical for which conditions?

Answer 11

• Constricting pain –> cardiac ischaemia or oesophageal spasm
• pain lasting over 15 mins and dull, central, and crushing –> ACS
• sharp pleuritic pain, catches on inspiration –> originates from pleura or pericardium –> pneumonia, pulmonary embolus or pericarditis
• sudden, substernal tearing pain radiating towards the back – > aortic dissection
• Precipitating factors:
  
  • Cardiac pain more likely with exercise or emotion, typically relieved with rest or nitrates
  • pain following fodd, lying down, alcohol or relieved by antacids –> GI cause
  • heartburn and acid regurg –> typical of GORD
• referred pain from abdominal pathology (e.g. acute cholecystitis and pancreatitis) will have associated symptoms
  
  • e.g. acute cholecystitis –> fever/ nausea/ vomiting/ severe upper R quadrant pain/ jaundice
  • acute pancreatits –> sudden onset, constant, radiation to back, worsen with movement, vomiting

Question 12

Differentials: Signs and symptoms

What are some atypical symptoms and typical symptoms for ACS?

Answer 12

• Typical: (along with central crushing pain that may radiate to jaw/ left arm)
  
  • dysponea
  • nausea and vomiting
  • sweating
• Atypical:
  
  • syncope
  • nausea/ vomiting or dysponea in abscence of chest pain
  • more common in women/ diabetics/ over 75 yrs

Question 13

Differentials: Signs and symptoms

What can associated dysponea with chest pain allude to?

Answer 13

Dysponea –> cardiac ischaemia, pulmonary embolism, pneumothorax, pneumonia

Question 14

Key features on clinical examination:

General features in cardiac exam

Answer 14

• Clubbing = congenital cyanotic disease (tetralogy of fallot), subacute infective endocarditis
• splinter haemorrhages = infective endocarditis
• peripheral cyanosis = cold hands and feet, occurs when there is peripheral vasoconstriction and blood stasis in extremities. Congestive heart failure, circulatory shock, raynauds
• central cyanosis =shunting of deoxygenated blood into systemic circulation e.g R- L shunt
• Also think, oedema, jaundice, pallor of mucous membrane cachexia and obesity

Question 15

Key features on clinical examination:

Rate and rhythm

Answer 15

Pulse: Rate and Rhythm

• 60- 100 bpm
• rhythm should be regular
• premature beats - occasional or repeated irregularities superimposed on regular rhythm or intermittent heart block as dropped beats
• atrial fibrillation - irregularly irregular pulse that persists with exercise (pulse irregularity due to ectopic beats usually disappears on exercise)

Question 16

Key features on clinical examination:

Pulse variations and clinical indication

Answer 16

• Carotid pulsation –> not normally visible but may be in high output conditions (e.g. fever/ anaemia/ thyrotoxicosis) and in aortic regurgitation
• collapsing/ water hammer pulse –> large volume pulse of short duration with a brisk rise and fall. Aortic valvular regurgation or persistent ductus arteriosus.
• Small volume pulse –> cardiac failure, shock, obstructive valvular or vascular disease or tachyarrhythmias
• Plateau pulse –> small in volume and slow in rising to a peak. Aortic stenosis.
• Alternating pulse –> alternate pulse weak followed by strong –> severe myocardial failure and indicates poor prognosis.
• Bigeminal pulse --> caused by ectopic beat after sinus beat, irregular rhythm with weaker pulse after first pulse caused by sinus beat.
• Pulsus bisferiens –> double pulse, first pulse caused by left ventricular contraction in systole (called percussion wave), second caused by a delayed recoil of the vascular bed as left ventricle empties slowly or is obstructed (tidal wave). Found in hypertrophic cardiomyopathy or mixed aortic valve disease.
• Dicrotic pulse –> accentuated dicrotic notch found in sepsis, hypovolaemic shock or aortic valve replacement.

Question 17

Key features on clinical examination:

JVP

Answer 17

• No valves between internal jugular vein and R atrium therefore JVP = good measure of R atrial pressure.
• elevation of JVP occurs in:
  
  • heart failure
  • constrictive pericarditis
  • cardiac tamponade (JVP increased during inspiration - Kussmaul’s sign).
  • renal disease w salt and water retention or excessive fluid transfusion
  • SVC obstruction
• reduced JVP occurs in hypovolaemia

Question 18

Key features on clinical examination:

Precordium

Answer 18

• with patient at 45 degrees, apex 5th IC space midclavicular line
• impalpable or displaced apex:
  
  • left ventricular dilatation will displace
  • impalpable in emphysema, obseity or pericardial or pleural effusion
• Tapping apex –> palpable first sound = mitral stenosis
• Vigorous apex –> volume overload eg aortic regurgitation
• heaving apex –> left ventricular hypertrophy, aortic stenoss, systemic HTN and hypertrophic cardiomyopathy
• double pulsation may occur in hypertrophic cardiomyopathy
• sustained left parasternal heave occurs in right ventricular hypertrophy or left atrial enlargement
• palpable thrill –> felt over abnormal valve

Question 19

Key features on clinical examination:

Auscultation of heart sounds

Answer 19

• 1st Heart sound = S1 –> due to mitral and tricuspid valve closure
• loud S1 occurs in thin people, tachycardias, mitral stenosis
• soft S1 occurs in obesity, emphysema, pericardial effusion, mitral stenosis or mitral/ tricuspid regurg, HF, shock, bradycardia and 1st degree heart block.
• 2nd Heart sound = S2 –> due to aortic and pulmonary valve closure
• May get physiological splitting of S2 in children and young adults.
• 3rd heart sound –> due to rapid ventricular filling, present in heart failure
• 4th heart sound –> late diastole, associated with atrial contraction
• singly or together they produce a gallop rhythm.

Question 20

Examination of angina pectoris

Answer 20

Typically normal in stable angina; rarely may find:

tachycardia

hypoxia

S3 sound - suggests ischaemia induced left ventricular dysfunction

mitral regurgitation murmur - suggests ischaemia induced papillary muscle dysfunction

babasilar crackles/ rales - suggests LV dysfunction

carotid bruit - atherosclerotic disease

diminished peripheral pulses - atherosclerotic disease

Question 21

Examination of ACS - what are common and uncommon signs?

Answer 21

Examination may be normal.

Common signs:

• 4th heart sound - due to reduced myocardial relaxation due to ischaemia
• diaphoresis (excessive sweating)
• nausea
• tachycardic or bradycardic (dependins on severity of ischaemia).
• carotid bruit - in atheromatous disease
• poor peripheral pulses - in atheromatous disease

Uncommon signs:

• Syncope
• 3rd heart sound - sudden blood flow into ventricles
• murmur - ischaemic valvular regurgitation
• Crackles - volume overload and compromised left ventricle

Question 22

Examination signs: Acute pericarditis

Answer 22

• Pericardial rub –> high pitched/ squeaky sound heard on ausculation of left sternal edge with patient leaning forward at end expiration
• sharp piercing/ stabbing pain over centre or left side of chest - more intense when breathing in
• relief of pain sitting up or leaning forward
• palpitations - which reflect change in cardiac rate or rhythm

Less common:

• Fever
• myalgias and malaise
• signs of R sided HF - fatigue, ankle oedema, and severe cases - ascities.

Question 23

Examination signs:

Aortic dissection

Answer 23

• Pulse deficit - reduction or abscence of pulse - common in proximal dissection affecting aortic arch, may be unilateral or bilateral
• diastolic murmur - aortic incompetence
• difference between L and R sided blood pressure - difference of BP between two arms is hallmark of aortic dissection
• features of ehlers danlos - hypermobile joints, translucent skin, easy bruising, premature ageing of akin
• marfan features - tall stature, arachnodactyly (long fingers/ toes), pectus excavatum, hypermobile joints, high arch palate, narrow face
• clinical signs of hypoperfusion

Question 24

Examination:

Pneumonia signs

Answer 24

• Decreased breath sounds - if one sided think pneumothorax, if focally think collapsed lobe
• crackles/ rales
• wheezing
• bronchial breath sounds - tubular, hollow sounds when auscultating large airways (2nd and 3rd IC spaces) - louder and higher pitched than vescicular breath sounds
• dullness to percussion
• increased tactile fremitus when severe consolidation

Question 25

Examination signs: Viral pleuritis

Answer 25

• Pleural friction rub w or without low grade dever

Question 26

Examination signs: Costochondritis

Answer 26

• Reproducible pain on chest wall palpation especially at costochondral junctions (junction between costal cartilage and rib bone)

Question 27

Examination signs: Herpes zoster

Answer 27

Tenderness unilaterally in a dermatomal distribution - with or without typical rash indicates herpes zoster (pain presents 2-3 days prior to rash)

Rash is vesicular on an erythematous base in unilateral distribution of one dermatome.

Question 28

Investigations:

Basic investigations chest pain

Answer 28

• Temperature, blood pressure, pulse, respiratory rate
• Heart rhthym
• oxygen saturation pulse oximetry
• Resting 12 lead ECG
• Make sure pain is controlled - any exacerabtions should be taken into account.

Question 29

What further investigations would be done if suspecting:

Angina pectoris 1st line

Answer 29

• Resting ECG - often normal in stable angina, but ST depressions may indicate ischaemia or Q waves indicative of prior infarction
• FBC - anaemia leads to additional cardiac workload and reduced O2 delivery to myocardiu, which exacerbates angina
• Fasting lipid profile - hyerplipidaemia associated with Ischaemic heart disease - elevated LDL = higher risk, elevated HDL = protective
• HbA1c or fasting blood glucose - hyperglycaemia linked to ischaemic heart disease

Question 30

What further investigations would be done if suspecting:

Angina pectoris - 2nd line

Answer 30

• TSH - hyperthyroidism increased metabolic demand and cardiac workload - can exacerbate angina. Hypothyroidism is associated with dyslipidaemia and ischaemic heart disease
• Stress exercise ECG - ECG before, during and after exercise, assess exercise capacity and heart rate achieved, haemodynamic response to exercise. - Looking for ST segement elevation and depression to identify ischemia.
• Imaging - stress plus CT/ echocardiogram/ cardiac magnetic resonance or stress positron emission tomography (PET). Imaging modality depends on patient demographic and qu. - To help identify wall motion or perfusion abnormalities
• CCTA - Cardiac computed tomographic angiography - British guideline recommended. Looking for luminal narrowing - > 50% considered positive or identification of plaques.
• Invasive coronary angiography - 50-70% luminal narrowing is considered coronary obstruction. Invasive coronary angiography not typically used for initial diagnosis but may be used to confirm, risk stratify, identify if appropriate for revascularisation.

Question 31

What investigations if suspecting:

ACS (STEMI/ NSTEMI/ Unstable Angina)

Answer 31

• ECG
  
  • ST elevation MI (STEMI) - ST elevation > 1mm in 2 anatomically adjacent leads or new left bundle branch block
  • NSTEMI or unstable angina –> ST segment depression or T wave inversion
• Trial sublingual glyceryl trinitrate - also control pain
• CXR
  
  • normal or signs of heart failure e.g. increased alveolar markings
  • blood diversion to upper lobes
  • cardiomegaly
  • pleural effusion
  • kerley B lines (septal lines) - interlobular septa become prominent due to oedema in the connective tissue inbetween lung lobes. Kerley B - often 1 - 2 cm in periphery of lung, extend out to pleural lining.
• Cardiac Enzymes (troponin and creatinine kinase MB)
  
  • ​elevated in STEMI and NSTEMI
  • Troponin released into blood 3-4 hours after MI, peaks 24 hrs, remains detectable for 10- 14 days
  • Troponin more specific but less useful to detect reinfarction
  • Creatinine kinase - rises 3/4 hrs after MI, remains elevated 3-4 days- useful to detect reinfarction
• FBC -> thrombocytopenia to estimate risk of bleeding
• U and E’s –> Urea and creatinine to monitor kidney function, electrolytes to monitor risk of cardiac arrhythmia
• LFT –> useful if considering tx with drugs that undergo hepatic metabolism
• Other investigations:
  
  • B type natriuretic peptide (BNP and NT-proBNP) - released during ischaemia, helps to risk stratify.
  • Coronary angiography - STEMI - critical occlusion of coronary artery, NSTEMI and unstable angina - evidence of coronary artery narrowing. STEMI- urgent coronary angiography with reperfusion. NSTEMI/UnstableA - if high risk features (ongoing chest pain, ECG changes, elevated cardiac enzymes).

Question 32

What investigations if suspecting:

Acute pericarditis

Answer 32

• ECG - upwards concave ST segment elevation with PR depressions (60% patients).
• Serum troponin - if raised suggests myocardial involvement and coincides with magnitude of ST segment elevation. Usually midly elevated, can be in range of acute MI.
• pericardial fluid/ blood culture –> purulent pericarditis is lifethreatening requires immediate confirmation via urgent pericardiocentesis. Pericardial fluid should be tested for bacterial/ fungal/ TB causes. Blood culture too.
• ESR - elevated consistent with inflammatory state
• CRP - elevated consistent with inflammatory stat
• Urea - elevated suggests uraemic cause- elevated above 21.4 mmol/L or 60 mg/dL suggests renal failure
• FBC - Leukocytosis - infectious cause
• CXR - usually normal unless large pericardial effusion - cardiothoracic ratio will be raised. Also looking for lung pathology.
• Echocardiography –> indicated when cardiac tamponade is suspected and differentiates from ACS. Looking to image pericardial effusion.
• can do Chest CT/ cardiac MRI –> echocardiogram inconclusive this can also detect pericardial effusion

Question 33

What investigations if suspecting: Pneumonia

Answer 33

• CXR - pulmonary infiltration, air bronchograms, pleural effusion
• WBC content
• sputum culture
• blood culture

Question 34

What investigations if suspecting: Aortic dissection

Answer 34

ECG - to exclude MI

CXR - may show haemomediastinum or pleural effusion - haemothorax

CT: tranverse cross section to show flap of aorta with true and false lumens.

Weakening or aortic wall leads to tearing of tunica intima which creates a flap. Blood fills this space and gradually continues to tear the tunica intima distally to the site of origin which forms a false lumen. Blood fills the medial layer of the aortic wall.

Echocardiography –> may show tamponade or aortic regurgitation

Transoeshophageal echocardiogram - can image entire thoracic aorta up except small portion of distal ascending aorta near arch.

Question 35

LO: Describe overview of principles of management of life threatening chest pain conditions :

What are LIFE THREATENING causes of chest pain?

Answer 35

• STEMI/ NSTEMI
• aortic dissection
• myocarditis
• pericarditis
• PE
• tension pneumothorax

Question 36

Management:

NSTEMI

Answer 36

NSTEMI:

• aims: relieve pain, identify and treat life threatening instability, relieve ischeamia, prevent further thrombosis or embolism, correct haemodynamic abnormalities
• Oxygen -> in pts that are hypoexamic, those in respiratory distress.
• Antiplatelet therapy –>
  
  • Aspirin - indicately immediated for pts with ACS (unless contraindicated)
  • P2Y12 receptor inhibitors (clopidogrel/ ticagrelor/ prasugrel) - inhibit platelet activation and adhesion/aggregation.
  • all patients should be placed on longer term dual antiplatelet therapy
• Pain relief
  
  • sublingual GTN –> reduced myocardial o2 demand and enhances oxygen delivery to myocardium (not given if R ventricular infarction or if recent phosphodiesterase 5 inhibitor use e.g. sildenafil (viagra))
  • intravenous GTN if 3 sublingual GTN doses ineffective
  • Intravenous morphine if pain continues
• Beta Blockers
  
  • used in all pts without contraindications
  • cardioselective preferred for initial tx - atenolol and bispropolol
  • post NSTEMI - metoprolol or bispropolol
• (Calcium channel blockers -> given to pts with continuing or recurrent ischaemic sx after nitrate and beta blocker therapy if ineffective )
• High risk patients need urgent coronary angiography and revascularisation if suitable
• high risk = continuous angina despite therapy, rise of cardiac markers, signs HF, arrhythmias, PCI within 6 month, prior CABG, renal dysfunction, diabetes, reduced LV function.
• Invasive approach - anticoagulation therapy (LMWH, UFH or fondaparinux ) and antiplatelet therapy before angiogram. PCI with angioplasty, alone or with a stent.
• conservative approach - anticoagulation tx plus aspirin and P2Y12 receptor inhibitor for 48 hrs. (LMWH, UFH, fondaparinux).

Question 37

Management of STEMI

Answer 37

*