AIP Flashcards
What do leads are present for anterior, lateral, inferior and posterior MI?
- V1, V2, V3 - LAD, anterior MI
- 1, aVL, V5, V6 - circumflex, lateral MI
- 2, 3, aVF, RCA, inferior MI
- V1, V2, V3 ST depression, RCA, posterior MI (also bradycardia)
What investigations needed for ACS?
o Observations including ECG
o Bloods
FBC, U+Es, LFTs and clotting, CRP
Troponins T and I (3x normal limit, rising), CK, AST, LDH
o Imaging
CXR to exclude differentials
What is the management of STEMI?
Morphine (for pain), cyclizine for nausea, oxygen if <94%, GTN 2mg unless hypo, aspirin 300mg oral and prasugrel (P2Y12 antag), unfractionated heparin before PCI(within 2 hrs)- transfer to CCU.
If fails or triple vessel - do CABG, graft from long saphenous vein or internal mammary artery
thrombolysis - 12 hour - alteplase - repeat ecg after 90min. <50% better = PCI needed still
Post MI complication? (DARTH VADER)
Death, Dressler’s, Arrhythmia, Aneurysm, Rupture, Recurrence, Tamponade, HF/CCF, Valve disease, Embolism
Fever, pleuritic pain relieved by leaning forwards, raised ESR
Dressler’s syndrome tends to occur around 2-6 weeks following a MI
Treated with NSAIDs
o Bradycardia
AVN block can occur following inferior MI as the RCA supplies the AVN leading to bradycardia
Persistent ST elevation
Aneurysm after MI
o Tamponade
Beck’s triad of raised JVP, low BP, muffled heart sounds
o Acute fall in BP
Cardiogenic shock following acute LVF - (inotropes and vasodilators eg. Noradrenaline)
o Systolic murmur and pulmonary oedema
Acute mitral regurgitation due to ischaemia of papillary muscle causing fluid backlog
POOR SOD (Pour away/stop fluids, sit up, oxygen, loop diuretic IV Furosemide)
Secondary prevention of MI (ABCDE)
o Conservative
Exercise, Mediterranean diet, less alcohol, smoking cessation, cardiac rehabilitation, HTN/DM management, avoid sex for 4 weeks, avoid driving for 4 weeks if not treated with PCI (1 week if treated with PCI)
o Medical ABCDE
Ace inhibitor Ramipril 10mg OD
BB (Atenolol)
Cholesterol (Atorvastatin 80mg OD)
Dual AP therapy (Aspirin 75mg OD for life + another antiplatelet (clopidogrel, ticagrelor, prasugrel) 12 months)
ECHO +/- Eplerenone Aldosterone antagonist eg. Eplerenone/Spironolactone if LV dysfunction (EF < 50% on echo_
NSTEMI and UA mangement
Conservative
* Scans (stress ECG, myocardial perfusion scan)
* GRACE score to determine risk of death or MI within 6 months)
* If low risk <3% then conservative
* Diet, exercise, cardiac rehabilitation, HTN/DM management
Medical
* Medium or high risk GRACE score >3%
o Aspirin plus Fondaparinux if PCI not planned immediately
o Then angiogram and PCI or CABG within 3 days/72 hours
When to do an angiogram?
* Hypotensive – immediate
* GRACE score >3% - angiogram within 3 days
* GRACE score <3% - angiogram after 3 days
Causes of Interstitial Lung Disease
Idiopathic Pulmonary Fibrosis
Iatrogenic
Nitrofurantoin, methotrexate, amiodarone
Inflammatory
Sarcoidosis -> Erythema nodosum, uveitis, hypercalcaemia
Infective
- TB
Toxins
- Coal, silicosis, asbestosis
- Farmers’, bird owner
Autoimmune
SLE, RA
What are the signs and symptoms of Interstitial Lung Disease?
- Signs and symptoms
o Gradual onset sob, non-productive cough, haematemesis, wheeze, chest pain, fever and myalgia
o Occupational history - smoking, farming, dust, birds, asbestos, coal
Examination
o Finger clubbing, cyanosis, wheeze, fine end-inspiratory crackles, tachycardia, RHF
What are the investigations needed for Interstitial Lung Disease?
Observations
Temp, BP, HR, RR, sats
o Blood tests
FBC, U+E, LFT, CRP, ESR
Antibodies RF, anti-CCP, ANA, dsDNA
Bedside
ABG, peak flow, spirometry, ECG
Restrictive pattern with FEV1/FVC > 0.7 and reduced total lung capacity
o Imaging
CXR, HRCT (honeycombing, nodular opacities, BHL, ground-glass changes), lung biopsy
Management of Interstitial Lung Disease?
o Conservative
Smoking cessation
Avoid triggers - dust, allergens, coal, asbestos, bird droppings
Seasonal influenza vaccinations
Physio
LTOT
o Medical
Corticosteroids (if symptomatic) - not for EAA
Pirfenidone (antifibrosis) - especially for IPF
o Surgical
Lung transplantation
What are the causes of PE?
Cause
o Thrombosis from DVT
o Fat embolism (surgery), amniotic fluid (pregnancy), tumour (cancer), air (trauma)
Pathophysiology
o Causes reduced blood flow to lungs resulting in VQ mismatch
o A massive PE will increase right ventricle afterload and cause right ventricular failure leading to haemodynamic compromise
PE presentation
Symptoms
Pleuritic pain and haemoptysis
Isolated SOB/dyspnoea/cough
Circulatory collapse and LOC (a massive PE)/light headedness
Signs
DVT (cause)
Hypotension, raised JVP, parasternal heave (RV failure)
Tachypnoea (most common sign), Tachycardia
Decreased O2 (VQ mismatch)
PE Investigations
NOTE: IF PE SUSPECTED, START DOAC IMMEDIATELY
Observations
Bloods: FBC, U&Es, LFTs, clotting, CRP, d-dimer, troponin
Bedside: ECG (Sinus tachycardia, S1Q3T3)
Wells PE is used to determine the investigations used
o D dimer IF WELLS SCORE IS <4
If negative, then stop DOAC
If positive, then CTPA or VQ
If PE suspected, start DOAC
If Wells PE <4, do d dimer
D dimer negative then stop DOAC
If Wells PE >4 or D dimer positive, then do CTPA (gold standard)
If CTPA contraindicated (renal impairment or contrast allergy) then do VQ scan instead
If CTPA or VQ is negative, stop DOAC
If CTPA or VQ is positive, continue DOAC
WELLs Score for PE
Wells PE is used to determine the investigations used
Suspected DVT: 3
PE most likely diagnosis: 3
Tachycardia: 1.5
3 days immobilisation in past 30 days: 1.5
Hx of thrombosis DVT/PE: 1.5
Haemoptysis/coughing blood: 1
Malignancy/cancer: 1
PE management
Immediate
A to E and stabilisation
Senior input as the patient is unwell
Conservative
If PESI score is low, can be managed as outpatient
Medical
Start DOAC immediately if PE suspected (Rivaroxaban, Apixaban)
* If provoked: 3 months DOAC
* If unprovoked: 6 months DOAC
IF ANTIPHOSPHOLIPID SYNDROME OR SEVERE RENAL IMPAIRMENT (<15/min): LMWH plus VKA (Warfarin) instead
IF MASSIVE PE WITH HYPOTENSION: thrombolysis with 50mg Alteplase bolus is first line
Surgical
IF REPEATED PEs: can try an IVC filter to stop clots getting into pulmonary circulation
PE in pregnancy management
PE in pregnancy
D-dimer cannot be used as it will be raised
If leg symptoms, do leg USS first
If PE suspected, do CXR
If CXR normal, do leg USS
If normal, do VQ scan (preferable to CTPA)
Consult obstetrician
What are the causes of COPD excarcebations
Most common cause is H.Influenza (annual influenza vaccine) and S.pneumoniae (one-off pneumococcal vaccine), or Moraxella
Rhinovirus is the most common viral cause
Investigations for COPD exacerbations?
Observations
* Temp, BP, HR, RR, sats
Routine bloods
* FBC, U+Es, LFTs and clotting, CRP
Bedside
* ABG, peak flow, ECG
Sepsis six and infection screen
* UOP, lactate, blood cultures, sputum culture
Imaging
* CXR
o If consolidation then pneumonia, otherwise infective exacerbation of COPD
What is the management of COPD Excacerbation
Immediate
* A to E assessment and stabilisation
* Senior input as this is an unwell patient
* 15L non-rebreathe mask if life threatening, otherwise Venturi titrated to 88 - 92% O2
* REPEAT ABG to assess for hypercapnic respiratory acidosis (need NIV)
Medical
* OSHIT AE (NV)
* Nebulised SABA salbutamol (2.5mg) +/- SAMA Ipratropium (0.5mg)
* Prednisolone 30mg for 5 days (40mg in Asthma exacerbation)
* IV theophylline with senior input
* Oral antibiotics ONLY IF purulent YELLOW or GREEN sputum or signs of pneumonia
o Amoxicillin (not if penicillin allergy) or clarithromycin (not if long QT syndrome) or doxycycline
* Non-invasive ventilation
o If respiratory acidosis <7.35, then NIV needed in an ITU setting (better outcomes than ET)
o Bilevel positive airway pressure with IPAP and EPAP
o Next step up could be intubation and ventilation
What are the different types of bowel ischaemia?
o Acute mesenteric ischaemia
o Chronic mesenteric ischaemia
o Ischaemic colitis
What are the causes of mesenteric ischaemia?
Mostly arterial embolus due to AF, as well as MI, IE
Venous due to hypercoagulation, tumours, infection
Also, non-occlusive due to hypovolaemia and blood vessel constriction (COCAINE –> acute mesenteric ischaemia)
Blocks the small bowel
Investigations for mesenteric ischaemia
Observations
Bloods – FBC, U+Es, LFT, CRP, lactate (ischaemic)
Bedside – urinalysis, ECG/echo
Imaging
* CXR and AXR (may show thumb printing due to oedema and inflammation)
* CT Angiography is gold standard
Management of mesenteric ischaemia?
Immediate
* A to E
* Senior input
* Morphine, Oxygen, anti-emetic, NBM
Medical
* Antibiotics
* Possibly thrombolytics or heparin
Surgery
* Embolectomy or angioplasty if bowel if viable
* Emergency laparotomy with resection usually required due to necrosis or sepsis