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Acutely Ill Patient > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q

What are the two main character types of chest pain?

A
  1. Somatic chest pain (originating from pericardium, pleura, chest wall) = well-localised, sharp
  2. Visceral chest pain (originating from cardiac muscle itself) = dull, aching, heavy /crushing
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2
Q

Common associated symptoms with chest pain…

A
  • Dyspnoea
  • Cough - respiratory cause?
  • Haemoptyisis - PE?
  • Nausea and vomiting
  • Sweating
  • Palpitations -arrhythmia?
  • Dizziness/ syncope
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3
Q

Difference between general inspection of cardiac chest pain and respiratory chest pain …

A
  • Cardiac chest pain = grey, clammy, unwell

- Respiratory chest pain = cyanosed, dyspnoaeic

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4
Q

What can be heard on auscultation in heart failure?

A
  • Cardio = gallop rhythm

- Chest = crackles indicating fluid on the lungs from pulmonary oedema

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5
Q

Differential diagnosis for chest pain…

A
  1. Cardiac : ACS (central crushing chest pain), pericarditis (pleuritic chest pain worse on lying down), stable angina (relived by rest), arrhythmia (palpitations), myocarditis
  2. Vascular: aortic dissection (tearing chest pain radiating to back between shoulder blades)
  3. Respiratory: PE (pleuritic chest pain, VTE risk factors), pneumonia (associated infective sx e.g. purulent sputum), pneumothorax (sudden pleuritic chest pain with SoB)
  4. Gastro: GORD (retrosternal burning chest pain, associated with eating) , oesophageal spasm, referred pain from cholecystitis, pancreatitis
  5. Other causes = shingles (dermatomal distribution across chest wall), panic disorder (associated with panic attacks)
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6
Q

Describe the pathophysiology of ACS?

A
  1. Endothelial injury: injury leads to inflammatory response leading to accumulation of LDLs which are then oxidised to reactive oxygen species.
  2. Plaque formation: These irritants then attract macrophages which phagocytose the LDLs to form fatty streaks.
  3. Plaque rupture: continued inflammation attracts smooth muscle cells which form a fibrous cap that then develops into an atheroma. The top of the atheroma forms a hard plaque which can rupture. This exposes a collagen-rich cap which causes platelets to aggregate on this exposed collagen, forming a thrombus.
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7
Q

Typical presentation of ACS…

A
  • Retrosternal, central crushing chest pain - radiates up the jaw and down left arm
  • Associated sx: nausea, sweating, palpitations, shortness of breath
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8
Q

What ECG changes are seen in STEMI ?

A

> Mins- hours: hyperacute T wave enlargement
0-12 hrs: ST segment elevation
1-12 hrs: Q -wave development (deeper and wider than normal)
Days: T-wave inversion
Weeks: T-waves will normalise, Q waves persist (sign of previous MI if already present)

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9
Q

What ECG changes are seen in NSTEMI/UA?

A

> ST segment depression

> T-wave inversion

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10
Q

What are the ECG criteria for thrombolysis in STEMI?

A
  • > 2mm in ST segment elevation in adjacent chest leads
  • > 1mm in adjacent limb leads
  • LBBB
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11
Q

What artery supplies the anterior aspect of the heart?

A

Left anterior descending artery (branch of LCA) ; supplies right ventricle, left ventricle and intraventricular septum

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12
Q

What artery supplies the lateral aspect of the heart?

A

Left circumflex artery (branch of LCA) which supplies left atrium and left ventricle.

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13
Q

What artery supplies the posterior aspect of the heart?

A

Right coronary artery distributed along posterior surface; supplies right atrium and right ventricle

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14
Q

What artery supplies the inferior aspect of the heart?

A

Right marginal artery which moves along right and inferior border of the heart ; supplies right ventricle and apex.

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15
Q

Anterior STEMI will show ECG changes in leads…

A
  • V1, V2, V3, V4 ST elevation

- Reciprocal ST depression in III and aVF

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16
Q

Lateral STEMI will show ECG changes in leads…

A
  • aVL, V5,V6 ST elevation

- Reciprocal ST depression in III and aVF

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17
Q

Inferior STEMI will show ECG changes in leads…

A
  • II, III and aVF ST elevation

- Reciprocal ST depression in I and aVL

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18
Q

Posterior STEMI will show ECG changes in leads…

A

V1, V2, V3 ST depression, with tall and wide R wave

*will most likely require additional V7,V8,V9 leads across the back for more detailed trace.

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19
Q

What else can cause ST elevation?

A
  • Pericarditis
  • Hyperkalaemia
  • Massive PE
  • Aortic dissection
  • Many of which can cause chest pain too!!
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20
Q

What blood tests should be requested for investigation of ACS?

A
  • FBC =in case of anticoagulant use
  • U&Es = baseline renal function for use of IV contrast in angiography
  • CRP= underlying infection
  • LFTs and clotting profile =bleeding risk if vascular intervention required
  • Cardiac enzymes = troponins, CK, AST, LDH
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21
Q

What are the guidelines for troponin levels in ACS management?

A
  • Troponin level taken at ED admission greater than 99th percentile (normal levels = <14ng/L)
  • Another measurement 3 hours later (needs to be a significant change seen)
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22
Q

Apart from troponin, what other cardiac enzymes are used for ACS diagnosis?

A
  • Creatinine kinase: returns to baseline within 48 hrs, so can identify re-infarcts
  • LDH
  • AST
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23
Q

What else can cause troponin rise?

A

Other causes of myocardial damage:

  • Tachyarrhythmia
  • Heart failure
  • Pericarditis
  • Chest trauma
  • Sepsis
  • Cardiomyopathy
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24
Q

Initial management of ACS…

A
  1. Aspirin 300mg PO and another antiplatelet (prasugrel 60mg/ticagrelor 180mg)
  2. High flow oxygen (only if hypoxic)
  3. IV access : Diamorphine 2.5-10mg + Metoclopramide 10mg
  4. GTN spray - unlikely to be effective in STEMI
    * *ECG within 10 minutes = identify subtype of ACS
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25
Q

Management of STEMI…

A
  • Primary PCI should be attempted within 120 mins of admission to ED (door to balloon time) , and within 12 hrs of sx onset
  • Patients receive dual antiplatelet before PCI (aspirin + prasugrel/ticagrelor) - as part of initial ACS management
  • During PCI there is additional antithrombotic therapy - UFH/ LMWH (additional agents incly glycoprotein IIb/IIIa inhibitors may be used if high thrombus burden)
  • If PCI is not available within 120 mins: fibrinolysis with IV alteplase/ reteplase, then transfer to PCI centre for rescue PCI within 12 hrs of sx onset
  • Patients presenting after 12 hrs of sx onset: enoxaparin/ fondaparinux
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26
Q

Management of NSTEMI/UA…

A
  • Dual antiplatelet therapy (aspirin + clopidogrel) - as part of initial ACS management
    Risk stratify using GRACE score (6 month mortality risk in NSTEMI/UA pts):
  • Intermediate - high (>3%)= angiography within 72hrs and dual antiplatelet therapy + Gp 2b/3a inhibitor
  • Low (1.5-3%) = dual antiplatelet therapy (300mg clopidogrel +300mg aspirin) and antithombotic therapy (fondaparinux)
  • Lowest (<1.5%) = life-long aspirin with f/u for a stress ECG
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27
Q

Complications of MI…

A

EARLY= LV dysfunction leading to:
- Pulmonary oedema - treated with high flow O2, diuretics
- Cardiogenic shock- treated with inotropes and vasodilators
LATER = weakening of myocardium due to necrosis:
- Mitral regurgitation
- VSD
- Cardiac tamponade

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28
Q

What should all patients with MI have before discharge?

A

Echocardiograpy - to look for LV dysfunction.

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29
Q

What are the driving restrictions post MI?

A

Patients should wait 4 weeks before they drive, unless they have had successful angioplasty - in which case they can drive after 1 week.

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30
Q

What medical management should be commenced post MI?

A

BAACS:

  • Beta blocker
  • Aspirin - lifelong
  • ACEi
  • Clopidogrel for 1 year
  • Statin
    (consider mineralocorticoid antagonist for pts with LV dysfunction post-MI)
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31
Q

What is GORD?

A

Presence of prolonged or excessive reflux of stomach contents into lower oesophagus.

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32
Q

What are the main causes of GORD?

A
  • Increased intrabdominal pressure: obesity, pregnancy
  • Reduced lower oesophageal sphincter (caused by obesity, fatty foods, alcohol)
  • Medications: SSRIs, NSAIDs, anti-cholinergics
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33
Q

What is the spectrum of GORD?

A
  • Non-erosive negative endoscopy reflux disease (NERD) =60% of patients
  • Oesophagitis (visual signs on endoscopy) = 35%
  • Complications = 5% - ulcerations, strictures, Barrett’s
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34
Q

How does GORD present?

A
  • Retrosternal burning chest pain - rising from stomach towards neck
  • Pain can be made worse by meals, lying down, bending over
  • Odynophagia (pain on swallowing)
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35
Q

What symptoms occur with dyspepsia?

A
  • Recurrent epigastric pain
  • Heartburn
  • Acid regurgitation
  • Bloating
  • Nausea and vomiting
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36
Q

How is GORD diagnosed?

A
  • Normally based on clinical findings and history
  • Therapeutic trial of PPI is then given without further investigation - (if it relieves sx, it is likely to be GORD)
  • Endoscopy is not recommended as most people will have no findings (60% = NERD) - barium swallow may show hiatus hernia, pH monitoring and manometry
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37
Q

When is endoscopy indicated?

A
  • Resistant dyspepsia (sx > 4 weeks despite medical management)
  • 2 week wait: New dysphagia/ abdominal mass/ >55y/o with weight loss and dyspepsia
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38
Q

Conservative management of GORD…

A
  • Weight loss
  • Smoking cessation
  • Reduction in alcohol intake
  • Raising head of the bed
  • Eating smaller portions
  • Not eating <3hr before bed
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39
Q

Medical management of GORD…

A
  • First line= PPI - 4 week course e.g. omeprazole 40mg OD, lansoprazole 30mg OD. If sx stop after 4-6 weeks, course can be discontinued.
  • Second line= H2 blockers
  • Prokinetics e.g. metoclopramide (increases speed of emptying)
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40
Q

When is H.pylori testing carried out?

A
  • If sx recur after PPI therapy, then a urea breath test is normally required.
  • Pt must be 2 weeks free of PPI therapy before test to prevent false -ve’s
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41
Q

What is the treatment for H. pylori infection?

A

TRIPLE THERAPY (PPI + 2 abx)

  • High dose PPI
  • Amoxicillin
  • Clarithromycin/ metronidazole
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42
Q

Surgical management of GORD…

A
  • Endoscopic gastroplication

- Laparoscopic fundoplication - used in hiatus hernia

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43
Q

What is a hiatus hernia?

A

Part of the stomach herniates through diaphragm into the thoracic cavity which leads to lower oesophageal sphincter becoming less competent, leading to reflux.

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44
Q

How does Barrett’s oesophagus occur?

A

Normal squamous epithelium of lower oesophagus changes to columnar epithelium (as found in the lining of the stomach).
There is increased risk of oesophageal adenocarcinoma–> surveillance endoscopy and PPI therapy

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45
Q

What are the main complications of GORD?

A
  • Oesophagitis
  • Barrett’s oesophagus
  • Peptic ulcer disease (gastric/ duodenal ulcers)
  • Oesophageal cancer
  • Benign peptic strictures
46
Q

What is a tension pneumothorax ?

A

Chest injury normally caused by trauma leading to a one-way valve forming in the pleural cavity. This leads to air entering the space with every inspiration but no air moving out.
Increasing intrathoracic pressure may cause significant mediastinal shift.

47
Q

What signs are seen in tension pneumothorax?

A
  • Tachycardia (compensating for decreased CO)
  • Pulsus paradoxicus
  • Hypotension
  • Tracheal deviation
  • Raised JVP
48
Q

How is tension pneumothorax managed?

A

Medical emergency that needs immediate treatment:

  • High flow oxygen
  • Wide bore cannulae into 2nd ICS mid-clavicular line.
  • Chest drain inserted immediately after relief of tension pneumothorax
49
Q

What is an open pneumothorax?

A

Caused by injury to the external chest wall which leads to an opening to the exterior.
Air moves into chest cavity preferentially through opening rather than trachea therefore ventilation is inadequate therefore lethal hypoxia occurs.

50
Q

How is open pneumothorax managed?

A
  • Chest wall defect must be covered with a bandage taped 3 times.
  • High flow oxygen
  • Chest drain insertion
51
Q

Causes of spontaneous pneumothorax…

A 
Primary= mainly found in tall, thin, young males -associated with Marfans 
Secondary = underlying lung disease e.g. COPD, CF, cancer, pneumonia, TB
52
Q

How does a pneumothorax present?

A
  • Sudden onset pleuritic chest pain
  • Dyspnoea
  • Exam findings: reduced expansion, hyper resonant percussion, reduced breath sounds
53
Q

What investigations are required for pneumothorax?

A
  • Oxygen saturation
  • Bloods: Clotting if chest drain is required , FBC and CRP for infection
  • ABG if SpO2 is low
  • CXR - measurement of intrapleural difference at hilum level so severity of pneumothorax can be calculated
54
Q

Management of pneumothorax…

A
  • Primary spontaneous:
    <2cm, no dyspnoea = discharge with follow up as O/P
    >2cm, dyspnoea = air aspiration and high flow oxygen - chest drain if aspiration is unsuccessful
  • Secondary spontaneous:
    > 1cm = admitted with high flow oxygen and aspiration
    >2cm, >55 y/o, dyspnoea - chest drain is required
  • Surgery: (for recurrent pneumothorax)
    Chemical pleurodesis
    Thoracotomy
55
Q

How does aspiration of air (thoracocentesis) take place?

A
  • Occurs in the triangle of safety
  • Maximum of 2.5L or to the point of pain/ resistance
  • > 2.5L aspiration may lead to re-expansion pulmonary oedema
56
Q

What are the borders of the triangle of safety?

A
  • Anterior edge of latissimus dorsi
  • Lateral edge of pectoralis major
  • 5th ICS - mid axillary line
57
Q

How is a chest drain inserted?

A

SELDINGER TECHNIQUE:

  • Puncturing chest wall with trochar (hollow needle) in triangle of safety, then passing guidewire through, withdrawing trochar and passing catheter over guidewire into pleural space before withdrawing guidwire.
  • Drain position is confirmed by imaging
  • Drain is then sutured in place
58
Q

Why should a bubbling chest drain never be clamped?

A
  • Bubbling chest drain = air still in the pleural cavity

- Clamping would lead to one-way valve causing a tension pneumothorax

59
Q

What are the complications of chest drain insertion?

A
  • Pain
  • Empyema - drain should be flushed daily to avoid infection
  • Drain dislodgement/ blockage
  • Surgical emphysema
60
Q

What are the main surgical interventions for pneumothorax?

A
  • Chemical pleurodesis: sterile talc inserted into pleural cavity to cause adhesions to form between pleural surfaces
  • Open thoracotomy and VATS (video assisted thoracoscopic surgery): resection of bullae and symphysis created between pleural surfaces
61
Q

What are the main causes of PE?

A
  • Thrombosis= most common
  • Fat embolus - following bone fracture/ orthopaedic surgery
  • Amniotic fluid
  • Tumour
  • Air
62
Q

What is the definition of a massive PE?

A

PE that causes haemodynamic compromise

63
Q

How does a PE cause haemodynamic compromise?

A

Large PE that occludes vascular bed –> increase in pulmonary artery pressue –> increased RV afterload leading to RV failure –>reduced pulmonary bloodflow –> reduced LV filling –>reduced cardiac output
*There is also hypoxia as a result of the V/Q mismatch caused by reduced pulmonary bloodflow

64
Q

Presentation of PE…

A

PE can present in 3 main ways:

  1. Pulmonary infarction: haemoptyisis, pleuritic chest pain
  2. Isolated dyspnoea
  3. Circulatory collapse with LoC

Examination findings: hypotension, tachypnoea, tachycardia, decreased SpO2, raised JVP, pleural rub

65
Q

Investigations for PE…

A
  • Oxygen sats - look for hypoxia and give high flow O2
  • Bloods : FBC, U+Es, LFT, INR, troponin (to rule out MI)
  • ECG: sinus tachycardia, RBBB, right axis deviation, S1Q3T3 (prominent S wave in V1, Q wave in V3, T wave inversion in V3)
  • CXR: linear atelectasis, raised hemidiaphragm, small effusion, wedge shaped infarct
66
Q

What is used for risk stratifying patients with PE?

A

Modified Well’s Score

  • Clinically suspected DVT = 3 points
  • Alternative diagnosis is less likely = 3 points
  • Tachycardia = 1.5 points
  • Immobilisation in past 4 weeks = 1.5 points
  • History of DVT/ PE = 1.5 points
  • Haemoptysis = 1 point
  • Malignancy = 1 point

Score >4 = PE likely

67
Q

How is PE diagnosed?

A

WELL’S SCORE > 4 = PE LIKELY:
Immediate CTPA –> -ve = PE excluded

WELL’S SCORE <4 = PE LESS LIKELY
D- dimer: -ve = alternative diagnosis, +ve = immediate CTPA

68
Q

What should be used in those with contraindication to CTPA (poor renal function/ contrast allergy)

A

V/Q SPECT or leg USS doppler

69
Q

Management of PE…

A

A-E assessment and management first!!
Similar to the management of DVT:
- Initially give LMWH or fondaparinux at diagnosis - then continue for 5 days or until INR > 2.0 for >48 hrs
- Warfarin/ DOAC should be started within 24 hrs - 3 months for provoked PE, or 6 months for unprovoked PE (i.e. no obvious cause like surgery)
*Thrombolysis is required in massive PE

70
Q

How is PE investigated and managed in pregnancy?

A

If PE is suspected - CXR:
- Normal CXR = USS doppler of the leg
- Abnormal CXR = V/Q scan (preferred to CTPA in pregnancy)
LMWH is commenced if PE is diagnosed - as warfarin is contraindicated.

71
Q

Why can d-dimer not be used in pregnancy?

A

D-dimer is a degradation product of fibrin - this is raised in pregnancy anyway due to fibrin deposition in the placenta.

72
Q

Causes of pleuritic chest pain…

A
  • Cardiac = MI, pericarditis
  • Respiratory = PE, pleural effusion, pneumothorax
  • Gastrointestinal = IBD
  • Rheumatological= Lupus pleuritic, rheumatoid arthiritis, Sjörgen’s syndrome
  • Infectious= Viral illness (most common) , pneumonia
73
Q

What is a pleural effusion?

A

Abnormal collection of more than 20ml of fluid within pleural space.

74
Q

Presentation of pleural effusion…

A

Symptoms:
- Shortness of breath - (mainly exertional)
- Dry cough
- Pleuritic chest pain
Signs:
- Reduced expansion and tracheal deviation (large effusion)
- Stony dull percussion
- Reduced breath sounds and decreased vocal resonance

75
Q

What are the main causes of pleural effusion?

A 
Transudative = <25g/L of protein:
- LV failure (heart FAILURE)
- Cirrhosis (liver FAILURE)
- Nephrotic syndrome , peritoneal dialysis (kidney FAILURE)
Exudative= >35g/L of protein: 
- Infection 
- Inflammation 
- Malignancy
76
Q

What is the difference between transudative and exudative effusion?

A

Transudative effusion has low protein content (<25g/L) because fluid is in the pleural space due to fluid being pushed OUT of capillaries by increased hydrostatic pressure (protein remains in capillaries).

Exudative effusion has high protein content (>35g/L) because it is made up of fluid that leaks out of capillaries due to oncotic pressure (moving from low to high conc) therefore protein moves across too.

77
Q

What investigations should be carried out for pleural effusions?

A

Oxygen saturation: if low, perform ABG
Bloods:
- FBC: increased WCC seen in infection
- U+Es and LFTs: renal/ liver failure can cause effusion
- CRP and ESR: inflammation/ infection
- Clotting screen: prior to chest drain insertion
- Amylase: pancreatitis
Imaging:
- CXR : blunted costophrenic angles and fluid level may be seen
- USS : increases success of pleural aspiration
- CT TAP: if there is high suspicion of malignancy

78
Q

What does malignant pleura appear like?

A
  • Thickened, nodular and thicker mediastinally

- If CT indicates malignancy - biopsy is required

79
Q

How does pleural aspiration occur, and what is tested?

A 
US guided procedure 
21 G needle and 50ml syringe is used 
Sample sent of for:
- Cytology: malignancy 
- Biochemistry: protein level, LDH, pH, glucose 
- Microbiology culture and sensitivity
80
Q

Characteristic pleural fluid findings…

A

With protein levels between 25 and 35, Light’s criteria should be used - the effusion is exudative if:

  • Pleural: serum protein > 0.5
  • Pleural: serum LDH > 0.6
  • Pleural LDH is > 2/3 upper limit of normal

High LDH = empyema, RA, malignancy
Low glucose = RA, TB, empyema
Blood staining = PE, mesothelioma, TB

81
Q

Management of pleural effusion…

A
  1. Pleural tap: removal of up to 1 L of fluid (more than this may cause reperfusion pulmonary oedema) - simple effusions will resolve after this
  2. Complex effusions (pH<7.2, turbid, culture +ve gram +ve) - need CHEST DRAIN
  3. Pleurodesis for recurrent effusion:
    - Medical= sterile talc for adhesion
    - Surgical = Pleurectomy and pleural abrasion
82
Q

Causes of empyema?

A
  • Commonest cause: parapneumonic effusion - bacteria gain access to effusion via lung parenchyma as a complication of pneumonia
  • Primary empyema caused by: aspiration, bronchial obstruction, oesophageal rupture
  • Secondary causes : TB, bronchiectasis, lung abscess
83
Q

Presentation of empyema…

A
  • Fever
  • Productive cough
  • Chest pain - pleuritic
  • Dyspnoea
84
Q

Investigations for empyema…

A
  • Oxygen saturation
  • Bloods : FBC (increased WCC), blood cultures, U+Es, LFTs, CRP, clotting screen (if chest drain is required)
  • CXR: blunted costophrenic angles and fluid meniscus
  • Pleural aspiration - 50ml under US guidance, sent for: cytology, biochemistry and microbiology
  • Contrast-enhanced pleural phase CT scan
85
Q

Management of empyema…

A

Antibiotics for at least 3 weeks:

  • Community accquired empyema= co-amoxiclav/ cephalosporin + metronidazole
  • Hospital accquired empyema= broad spectrum e.g. meropenem/ vancomycin

Chest drain - will require anticoagulation prior to this
Surgery if sx persist beyond 7 days

86
Q

Potential causes of acute pericarditis…

A
  • Primary idiopathic disease (commonest)

- Secondary causes: infection (coxsackievirus), SLE, uraemia, malignancy, Dressler’s syndrome, radiation

87
Q

Presentation of acute pericarditis…

A
  • Pleuritic chest pain made worse on lying down, relieved by sitting forwards
  • Dry cough
  • Dyspnoea
  • Pericardial rub heard on auscultation - v. specific
  • Likely to follow on from viral infection - flu-like prodrome may be present
88
Q

What investigations are carried out in acute pericarditis?

A
  • Blood tests: FBC, ESR, CRP, U+Es, troponins
  • Rheumatological screen if sx last longer than a week
  • ECG: PR depression (v specific), T-wave inversion, ST saddle elevation (widespread)
  • CXR: enlarged, globular heart
  • Echo: small pericardial effusion seen
89
Q

Management of acute pericarditis…

A

Treat the underlying cause!

  • High dose NSAID e.g. naproxen 250mg QDS along with Colchicine = 1st line therapy
  • PPI to be given as gastro protection
  • Glucocorticoids used in refractory pericarditis
90
Q

How does constrictive pericarditis occur?

A

Occurs as a consequence of injury to the pericardium.
Usually caused by any cause of acute pericarditis - mainly TB or malignancy.
*Leads to stiffness and lost of elasticity of the pericardial sac.

91
Q

Presentation of constrictive pericarditis…

A
  • Dyspnoea
  • Right heart failure: raised JVP , ascites, oedema , hepatomegaly
  • Kussmaul’s sign= paradoxical rise in JVP on inspiration
  • Pericardial knock - S3 (loud early diastolic sound caused by ventricular filling being limited by stiff pericardial sac)
92
Q

What does CXR show in constrictive pericaridtis?

A

Pericardial calcification and thickening

93
Q

Management of constrictive pericarditis…

A
  • NSAID therapy - few months

- Surgery is normally required: pericardectomy - surgical removal of portion/ all of pericardial sac

94
Q

Causes of cardiac tamponade…

A
  • Pericarditis
  • Aortic dissection
  • Ventricular rupture - may be caused by trauma, post MI
  • Iatrogenic - e.g.cardiac catheterisation
95
Q

Presentation of cardiac tamponade…

A
  • Beck’s triad: hypotension, raised JVP, muffled heart sounds
  • Tachycardia
  • Dyspnoea
  • Pulsus paradoxus (pulse drops during inspiration)
96
Q

What investigations are carried out and what findings are seen in cardiac tamponade?

A
  • CXR: enlarged globular heart - cardiac silhouette is large
  • ECG: electrical alternans (alternating amplitude of QRS complexes) , and low amplitude QRS
  • FAST scan is investigation of choice in trauma - echo may not be available in the acute setting.
97
Q

Management of cardiac tamponade…

A
  • A-E assessment is required!
  • Venous return and cardiac output improved by raising legs and positive inotropic drugs ( increase contractility)

DEFINITIVE TREATMENT:

  • Thoracotomy in theatre is ideal: drain pericardial fluid
  • In acute setting echo-guided pericardiocentesis may be definitive therapy
98
Q

Causes of oesophageal rupture…

A
  • Boerhaave syndrome (severe vomiting or straining leading to spontaneous perforation of oesophagus)
  • Trauma
  • Iatrogenic (endoscopy/ biopsy)
  • Ingestion of corrosive substances
  • Foreign body
  • Carcinoma
99
Q

Presentation of oesophageal rupture…

A 
Symptoms:
- Severe chest pain
- Dysphagia 
- Odynophagia 
- Pyrexia 
Signs:
- Surgical emphysema in supraclavicular area
- Tachycardia 
- Cyanosis
100
Q

Investigations for oesophageal rupture…

A 
Blood tests: 
- FBC (raised WCC)
- ABG (acidosis)
Imaging:
- CXR (pleural effusion, pneumomediastinum) 
- Barium swallow
- CT scanning
- Upper GI endoscopy - when other imaging is negative but suspicion is strong
101
Q

Management of oesophageal rupture…

A
  • NBM for at least 5 days from point of diagnosis
  • Parenteral nutrition
  • NG suction
  • IV antibiotics
  • Surgery may be necessary - debridement of mediastinum
102
Q

How does aortic dissection occur?

A

Tear in the tunica intima of the wall leads to blood accumulation and separation of the layers -blood is found between the intima and muscularis, or between muscularis and serosa.

103
Q

Risk factors for aortic dissection…

A

**HYPERTENSION = most important risk factor
Smoking
Dyslipidaemia
Aortic valve disease
Connective tissue disorders: EDS and Marfan’s syndrome
Trauma
Pregnancy

104
Q

What is the classification of aortic dissection?

A
  • Type A: involves the ascending aorta - requires cardiothoracic input due to risk of proximal spread causing tamponade
  • Type B: does NOT involve ascending aorta - mainly descending aorta which is distal to L subclavian vein
105
Q

Presentation of aortic dissection…

A
  • Sudden onset severe tearing chest pain that radiates through to back
  • Hypertension
  • Aortic regurgitation
  • Inferior MI

Symptoms dependent on artery involvement:

  • Coronary artery = angina
  • Spinal artery = paraplegia
  • Distal aorta = limb ischaemia
106
Q

Examination findings in aortic dissection…

A
  • Difference in BP on both arms (>15mmHg SBP)

- Signs of heart failure (caused by severe aortic regurgitation) : bibasal crackles, increased JVP

107
Q

Investigations for aortic dissection…

A
  • Bloods: troponins, D-dimer, cross-match several units
  • ECG: rule out MI
  • CXR: mediastinal widening
  • Transoesophageal USS : very sensitive for diagnosing and showing extent of damage.
108
Q

Management of aortic dissection…

A

Management is dependent on classification:
- Type A= surgical intervention - endovascular/ open aortic repair and graft insertion. BP controlled - target of 100-120 systolic

  • Type B= medical management with aggressive BP control - IV labetalol.
109
Q

What is shingles, and what causes it?

A

Unilateral, painful blistering rash caused by reactivation of the Varicella Zoster Virus (VZV) within a nerve root, leading to dermatomal distribution.

110
Q

Presentation of shingles…

A
  1. Days before the classical rash, there may be other symptoms:
    - Headache
    - Burning, tingling sensation
    - Generally unwell feeling
    - High temperature
  2. This is followed by pain - may be band like across the chest, and burning/ dull in sensation. Affected area may remain tender for some time.
  3. Rash that develops with itchy blisters/ vesicles - may last for a week.
111
Q

Management of shingles…

A

First line= Oral acyclovir - will reduce the post-herpetic neuralgia

112
Q

What is the shingles vaccine, and what contraindications are there?

A

Live attenuated vaccine offered to all patients aged 70-79 years old.
Contraindications= immunosuppression

Acutely Ill Patient (16 decks)

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