Acute Central Chest Pain Flashcards

1
Q

What are the common causes of acute central chest pain?

A

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

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2
Q

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

A
  • 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
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3
Q

Demographics and risk factors for ACS?

A
  • 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.
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4
Q

What are the risk factors for pericarditis?

A
  • 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
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5
Q

Risk factors for pneumonia?

A
  • 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
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6
Q

viral pleuritis RF

A

Cocksackie B viral infection

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7
Q

Risk factors for costochondritis

A
  • microtrauma - recent history of coughing or unaccostomed repetitive upper limb movement
  • women
  • over 40 yrs
  • hispanic
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8
Q

RF for GORD

A
  • 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
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9
Q

RF for generalised anxiety

A
  • 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
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10
Q

Focused history of acute central chest pain:

A

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

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11
Q

Differentials: Signs and symptoms

How can pain present differently?

what pain presentations are typical for which conditions?

A
  • 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
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12
Q

Differentials: Signs and symptoms

What are some atypical symptoms and typical symptoms for ACS?

A
  • 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
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13
Q

Differentials: Signs and symptoms

What can associated dysponea with chest pain allude to?

A

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

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14
Q

Key features on clinical examination:

General features in cardiac exam

A
  • 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
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15
Q

Key features on clinical examination:

Rate and rhythm

A

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)
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16
Q

Key features on clinical examination:

Pulse variations and clinical indication

A
  • 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.
17
Q

Key features on clinical examination:

JVP

A
  • 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
18
Q

Key features on clinical examination:

Precordium

A
  • 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
19
Q

Key features on clinical examination:

Auscultation of heart sounds

A
  • 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.
20
Q

Examination of angina pectoris

A

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

21
Q

Examination of ACS - what are common and uncommon signs?

A

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
22
Q

Examination signs: Acute pericarditis

A
  • 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.
23
Q

Examination signs:

Aortic dissection

A
  • 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
24
Q

Examination:

Pneumonia signs

A
  • 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
25
Q

Examination signs: Viral pleuritis

A
  • Pleural friction rub w or without low grade dever
26
Q

Examination signs: Costochondritis

A
  • Reproducible pain on chest wall palpation especially at costochondral junctions (junction between costal cartilage and rib bone)
27
Q

Examination signs: Herpes zoster

A

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.

28
Q

Investigations:

Basic investigations chest pain

A
  • 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.
29
Q

What further investigations would be done if suspecting:

Angina pectoris 1st line

A
  • 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
30
Q

What further investigations would be done if suspecting:

Angina pectoris - 2nd line

A
  • 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.
31
Q

What investigations if suspecting:

ACS (STEMI/ NSTEMI/ Unstable Angina)

A
  • 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).
32
Q

What investigations if suspecting:

Acute pericarditis

A
  • 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
33
Q

What investigations if suspecting: Pneumonia

A
  • CXR - pulmonary infiltration, air bronchograms, pleural effusion
  • WBC content
  • sputum culture
  • blood culture
34
Q

What investigations if suspecting: Aortic dissection

A

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.

35
Q

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

What are LIFE THREATENING causes of chest pain?

A
  • STEMI/ NSTEMI
  • aortic dissection
  • myocarditis
  • pericarditis
  • PE
  • tension pneumothorax
36
Q

Management:

NSTEMI

A

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).
37
Q

Management of STEMI

A

*

38
Q
A