Thorax Flashcards

Question

What are the diaphragmatic orifices and what goes through them?

Answer 1

Caval hiatus (T8) = IVC + R phrenic Oesophageal hiatus (T10) = oesophagus, CNX + oesophageal branches of L/R gastric a/v Aortic hiatus (T12) = aorta, thoracic duct + azygous vein 2, 3 and 3

Answer 2

Double-domed musculotendinous sheet located at inferior aspect of rib cage seperating thorax/abdomen and allowing respiration Right crus arises from L1-3 vertebra (LOS) - R dome lies higher than L due to liver Left crus arises from L1-2 Muscle fibres fuse to form central tendon that connects to inferior fibrous pericardium 3 peripheral attachments: 1. Lumbar vertebrae + arcuate ligament 2. CC 7-10 + directly to ribs 11-12 3. Xiphoid proccess Innervation: - Phrenic n (cervical plexus C3-5) - Inf. phrenic arteries

Answer 3

1. Intercostals: external (inferoanteriorly continuous with EO), internal (inferoposteriorly continuous with IO) & innermost (alike internals) - intercostal nerves (T1-11) Neurovasculature bundle runs between internal & innermost on inferior aspect of rib in the order VAN (sup to inf) 2. Transversus thoracis (continuous with TA) - intercostal nerves (T2-6) 3. Subcostales (like innermost fibres) - intercostal nerves

Answer 4

Action: protect thoracic viscera 1. Manubrium: concave producing jugular notch then lateral articulation with SC joint + facet for 1st rib CC & demifacet for 2nd rib CC -> sternal angle T4/5 between manubrium + body called the manubriosternal joint (count ribs from CC 2 here) 2. Body: articular facets for CC ribs 3-6 + demifacets for 2nd + 7th rib Xiphisternal joint 3. Xiphoid: tip @ T10 - largely cartilaginous and ossifies by age of 40

Answer 5

Typical rib = head, neck + body Articulates with the corresponding vertebra and the one above Each rib has costotransverse (rib tubercle to transverse costal facet of vertebra) & costovertebral joint (rib head, sup. costal facet of corresponding vertebra & inf. facet for vertebra above) Ribs 1-7 attach to sternum 8-10 attach to CC superior to them 11-12 end in abdominal musculature & do not have anterior attachment Atypical ribs = 1, 2, 10, 11 & 12 1 = shorter/wider with only 1 facet + has 2 grooves for subclavian vessels 2 = thinner/longer + serratus anterior attachment point 10 = 1 facet 11/12 = no neck + 1 facet

Answer 6

Lateral sternal border to MAL spanning 2nd-6th CC's - axillary tail runs along inferolateral edge of pec major to axillary fossa Mammary glands (modified sweat glands) consisting of series of ducts + secretory lobules 15-20 -> each consists of alveoli drained by single lactiferous duct converging at nipple - surrounded by fibrous (forms suspensory ligament of cooper) & fatty tissue Base lies on pectoral fascia attached by ligament + the space between this and the connective tissue is the retromammary space Blood supply: - ITA (medial) & thoracic/thoracoacromial (post. ICs)/mammary (ant. ICs)(lateral) - Veins correspond & drain into axillary & internal thoracic veins Nerve supply: ant/lat cutaneous branches of 4-6th IC nerves (sensory & autonomics) Lymphatic drainage: 1. Axillary nodes 2. Parasternal nodes 3. Post. IC nodes

Answer 7

Inflammation of the endocardial surfaces of the heart including valves usually due to microorganisms e.g. S. Viridans, coagulase - Staph, enterococci or HACEK Types: 1. Infective (acute/subacute): friable vegetations forming large irregular destructive masses on valve leaflet & adjacent structures 2. RHD: small warty vegetations along line of valve closure 3. Non-bacterial thrombotic/marantic: due to adenoCas for e.g. small-medium nondestructive vegetations at line of valve closure 4. Libmans sacks: due to adeno Cas for e.g. with small-med inflammatory vegetations either side of valve leaflet Macroscopic findings: aschoff nodules & fibrinoid necrosis Microscopic findings: aschoff bodies in all 3 heart layers (granulomatous inflammation with central zone of degenerating ECM infiltrated by immune cells inc. Anitshkow/caterpillar cells = activated macrophages with wavy nuclear outline)

Answer 8

1. Host immune response to GAS cross-reacting with host proteins e.g. Abs/CD4+ T cells direct Abs to M proteins that recognise cardiac self Ags 2. Complement activation, PMNs activated + cytokines damage heart tissue via Ab/T cell reactions 3. Recurrent inflammation causes fibrosis, narrowing & stiffening of valve leaflets 4. Chronic stage: commisural fusion (Fused chordae tendinae), retraction of edges, thickening, calcification & stenosis 5. Turbulent blood flow increases risk of bacterial colonisation on damaged tissue causing IE

Answer 9

Diagnostic for IE if 2 major criteria (or 1 major, 3 minor or 5 minor) Major: 1. BCs + for endocarditis from 2 seperate samples 2. Echo positive for IE findings e.g. valvular vegetations, leaflet nodules, chordal elongation/rupture, annular dilatation & pericardial effusion Minor: 1. Predisposition e.g. IVDU 2. Vascular phenomena e.g. janeway lesions 3. Microbiology evidence but not classic 4. Fever >38 5. Immunologic phenomena e.g. Roth spots 6. Echo findings atypical

Answer 10

Cardiac - AMI - Pericarditis - HF - Arrythmia Non-cardiac - GN - AKI - Stroke - Mesenteric infarct

Answer 11

Fever Roths spots Oslers nodes (painful finger nodules) Murmur Janeway lesions (palm) Anaemia Nail haemorrhage Emboli

Answer 12

IV Abx depending on MCS for 6 weeks e.g. IV Ceftrixone & Vancomycin Limitations: valves do not have specific blood supply, organisms lie inside vegetations & biofilm protects bacteria Surgical if no response -> 1. Valve replacement: mechanical (long-lasting/durable), tissue, Ross procedure (borrowing healthy valve + moving it) & TAVI/TAVR/balloon valvuloplasty* 2. Heart transplant (HLA matching needed) *if occurs on valve replacement already it will need to be removed as its a septic focus + will be dehiscent

Answer 13

Immunosuppressants: 1. Corticosteroids e.g. pred -> anti-inflammatory & kills T cells 2. Cytotoxics e.g. mycophenolate -> block cell division 3. Immunophilins e.g. ciclosporin -> blocks T cell responses 4. Lymphocyte depleting therapies e.g. monoclonals -> kills activated T cells

Answer 14

1. Lipid accumulation causes inflammation, calcification, valve thickening & stenosis - can be due to post-inflammatory scaring (RHD), senile calcification or if valve is congenitally bicuspid its prone to calcification 2. Sclerosis is before there is obstruction then this progresses to stenosis so LV encounters chronic resistance to systolic ejection increasing afterload -> LVH 3. Decreased LV elasticity + coronary blood flow increasing myocardial workload, O2 consumption & mortality -> can cause MI & sudden death 4. Later LV chamber shrinks, decreasing preload too, worsening systolic function causing insufficient SV/CO/EF causing HF & backward transmission to lungs causing pulmonary HTN

Answer 15

Solid material formed from constituents of blood in flowing blood = healthy response to injury intended to prevent bleeding 1. Atheromatus plaque ruptures due to haemorrhage within it exposing sub-endothelial collagen + necrotic plaque contents to blood 2. Platelets adhere, aggregate & activated releasing thromboxane A2, ADP & 5HT causing further aggregation & vasospasm 3. Coagulation activated by TF exposure + thrombus grows to a point where within minutes it can completely occlude artery 4. Aerobic glycolysis ceases dropping ATP + noxious metabolites accumulate in cardiac myocytes 5. Rapid loss of contractility within minutes of ischaemia & ultrastructural changes occur e.g. cell/mitochondrial swelling - potentially reversible 6. If lasts 20-40 mins irreversible damage & myocyte death occurs -> coagulation necrosis

Answer 16

Candida Aspergillus Tricophyton Microsporum

Answer 17

Mechanical have excellent durability, are easy to insert but thrombo-embolism/bleeding risk & need Warfarin Tissue valves are noiseless, do not need warfarin due to low thrombo-embolism/bleeding risk but insertion is more difficult

Answer 18

1 = lateral to pec minor 2 = deep to pec minor 3 = medial to pec minor Also classified into lateral (humoral), anterior (pectoral), posterior (subscapular), central which all drain into apical nodes -> subclavian trunk

Answer 19

Whole body except right UL, breast, lung, head & neck which goes to right lymphatic duct

Answer 20

Higher plasma growth hormone levels in patients with lung Ca Platelets clusters lodge in peripheral vasculature of digits release PDGF leading to increased permeability, vascularity & connective tissue changes

Answer 21

Fluorescence in situ hybridisation - cytogenetic technique using fluorescent probes binding chromosome parts to show high degree of sequence complementarity

Answer 22

Cancer of mucus secreting glands

Answer 23

Lung condition developed in smokers often causing SOB due to alveoli damage causing the air sacs to weaken/rupture creating larger air spaces instead of smaller ones

Answer 24

Symptom complex that occurs in patient with cancer that is not explained by local/distant spread or hormonal effects of the tissue of tumour origin Examples: - HyperCa & pancoast tumours e.g. SCC of lung due to PTHrP - Cushings, Lambert-Eaton Mysathenic syndrome & SIADH e.g. SCLC - HOAP & Trousseaus (venous thrombosis) e.g. adenoCa of lungs

Answer 25

MC+S for sputum using Ziehl-Neelson staining (takes 1-8 weeks) - using solid media (Middlebrook) or liquid (BACTEC/MIGT) PCR Interferon gamma assays FNAC of LN (necrotic tissue, histiocytes & giant cells) Mantoux skin test to test immunity Need to be labelled as category B in biohazard bag

Answer 26

- Notify communicable disease consultant - Avoid working in food factory - Use mask during sneeze/cough - DOTS (directly observed treatment short-course) anti-TB therapy - Contact tracing, screening & treatment

Answer 27

Organised collection of macrophages fusing to form Langerhan giant cells - composed of necrotic centre surrounded by T and B cells Other causes: Sarcoidosis RA Crohns Leprosy

Answer 28

Well circumscribed plaques of dense calcified collagen on X-ray - most common manifestation of asbestos exposure Increase risk of mesothelioma & adenoCa

Answer 29

1. Liquefactive 2. Caseous 3. Fibrinoid 4. Fat 5. Gangrenous 6. Coagulative

Answer 30

History/exam: risk factors Imaging (USS in <40yo + men): speculated mass & microcalcifications Biopsy (tru-cut/FNAC): C4-5 indicates suspicious to malignant When reviewing pathology assess: 1. Type of cancer 2. LN involvement 3. Hormonal status 4. Margins status

Answer 31

IDC of upper outer quadrant (more glandular tissue)

Answer 32

Human epidermal growth factor receptor 2 Oncogene and biomarker overexpressed in 15% of cases and associated with poor prognosis as less likely to be responsive to hormonal therapy, spread faster and recur IHC: measures amount FISH: measures no. of copies of the gene Management: Traztuzumab (Herception) is a monoclonal Ab that causes destruction of cells overproducing HER2

Answer 33

Nose: mupirocin 2% nasal ointment TDS for 5/7 Skin: wash OD with Chlorhexidine 4% for 5/7 Hair: same Chlorhexidine wash on day 1 and 5

Answer 34

Looks like eczema around nipple but will start at the nipple and progress out DCIS extension up lactiferous ducts and into nipple skin causing crusting exudate over nipple and areolar

Answer 35

Fibroadenoma - "breast mouse" Proliferation of epithelial and stromal tissue of duct lobules Often mobile, oval & rubbery presenting in upper outer quadrant <5cm Mx: can be excised but can be left alone - should still undergo TRIPLE ASSESSMENT

Answer 36

Biphasic breast lesion larger than fibroadenoma presenting in females 40-50 caused by overgrowth of stromal components - tend to grow rapidly Histologically may show: morphologic heterogenity, irregular gland dilatation, stromal mitotic activity & stromal cytological atypia Mx: WLE or mastectomy as can be aggressive

Answer 37

Fluid filled distended involuted lobules developing in peri-menopausal women Smooth/discrete/painless Mx: imaging will confirm, can be aspirated but if bloody will need triple assessment

Answer 38

1. Cyclical: B/L - caused by exaggerated response to hormonal changes causing enlargement & nodularity 2. Non-cyclical e.g. due to meds, contraceptives, antidepressants & antipsychotics 3. Extramammary e.g. chest/shoulder pain Mx of 1: better fitting bras, soft supportive bra at night, pain diary, analgesia & Danazol (anti-gonadotrophin) if not responsive to basic measures

Answer 39

1. Lactational: in first few weeks or during weaning as babies teeth cause trauma & crack skin 2. Non-lactational e.g. periductal mastitis in young females who smoke due to inflammation of subareolar ducts (nipple retraction, discharge, lump behind nipple, painful, tender, erythematous) Most commonly S Aureus, S epidermidis or Strep species Mx: urgent USS, I+D then MC+S of fluid - lactating women should continue to feed or express

Answer 40

Sclerosing thrombophlebitis of superficial veins of breast & chest wall Sudden onset pain with tenderness of subcutaneous red cord of tissue which will become painless eventually Mx: NSAIDs but may take months to settle

Answer 41

Enlargement of male breast tissue due to imbalanced oestrogen to androgen activity (B/L or U/L) Causes: Physiological Medication e.g. Spironolactone Testicular Ca e.g. leydig (increased oestrogen) Klinefelters (lack of testosterone) Mx: triple assessment, USS & treat underlying cause if there is one

Answer 42

Colour - blood stained B/L or U/L Arising spontaneously or on expression Lump Hx of breast disease Causes: - Physiological: any colour + no Mx needed - Galactorrhoea: B/L milk but check prolactin to r/o pituitary prolactinoma - Duct ectasia: perimenopausal women due to shortening/dilatation of sub-areolar ducts causing creamy/blood stained discharge so excise duct to r/o malignancy - Intra-ductal papilloma: serous/blood-stained +/- lump increases Ca risk

Answer 43

Risk factors Non-modifiable: family Hx, male & age Modifiable: smoking, DM & hyperlipidaemia 1. Endothelial injury from risk factors leading to increased permeability, leukocyte adhesion & thrombosis 2. Accumulation of lipoproteins in vessel wall (oxidised LDL + cholesterol crystals) 3. Platelet adhesion 4. Monocyte adhesion, migration into intima & differentiation into macrophages 5. Lipid accumulation in macrophages = foam cells releasing inflammatory cytokines 6. SMC recruitment due to factors released from platelets, macrophages & vascular wall 7. SMC proliferation & ECM production

Answer 44

Acute diffuse inflammatory lung injury that causes non-cardiogenic pulmonary oedema characterised by hypoxaemia, decreased lung compliance and diffuse pulmonary infiltrates In acute phase: 1. Widespread destruction of capillary endothelium, extravasation of protein rich fluid & interstitial oedema 2. Neutrophil migration & cytokine release 3. Alveolar BM damaged so fluid seeps into airspaces, stiffening lungs & causing V/P mismatch In chronic phase: fibroproliferation, organisation of tissue & disordered collagen deposition can cause lung scarring -> impaired gas exchange with refractory hypoxaemia, decreased compliance & pulmonary HTN Causes: 1. Sepsis 2. TRALI 3. CAP/HAP 4. Aspiration 5. Burns

Answer 45

Berlin criteria taking into account: PAO2/FIO2/carrico index shows the partial pressure of arterial oxygen over the inhaled oxygen comparing O2 in blood to that breathed in to assess if there is a problem with lungs transfer of O2 to blood

Answer 46

Supportive in ITU 1. Airway/breathing support: prone positioning & PEEP of 5-15cm H2O 2. Low dose steroids 3. Abx in sepsis 4. Strict IP/OP + invasive monitoring of pulmonary capillary wedge pressure to guide IVF OR consider inotropes OR diuretics 5. Nutritional support ideally enteral 6. VTE 7. PPIs prophylactically

Answer 47

Sepsis may induce pre-term labour so we would cure this but the surgery may cause the same, IUFD or VTE Neonatologist, obstetricians, obstetrics HDU to be involved Likely will need to be positioned laterally + raised legs (reverse trendelenberg) to improve VR/preload and prevent IVC compression

Answer 48

Amount of myocardium stretched after diastole (this is why you need to bolus not just speed up fluid) BP = SVR X CO (HR x SV) When BP is low, the preload is reduced and as per Frank-Starling mechanism this reduces cardiac output so the body will use: 1. Baroreceptors at aortic arch/carotid sinus (CNXI - sinus n. of Herring) activate sympathetics: tachycardia, increased SV & vasoconstriction to increase CO* 2. RAAS system: renin released from macula densa of JGA to cause salt/water retention + cortisol from adrenal cortex releases cortisol to increase BP 3. Catelcholamines: adrenal medulla stimulated by pain/injury causing increased SVR due to NA *This also happens simply on standing up to maintain BP

Answer 49

Circulatory failure whereby the body cannot perfuse the organs well enough to meet the demands

Answer 50

1. Muscle contraction via pump mechanism e.g. TEDs + intermittent pneumatic compression devices 2. Decreased venous compliance via sympathetic activation, increases CVP + improves blood flow 3. Respiratory activity - increased during inspiration due to reduced right atrial pressure 4. Gravity + VC compression decreases it Mx inc. IVF, inotropes or vasopressors: - Vasopressors: adrenergic agonists e.g. A/NA increase SVR via vasoconstriction, HR/SV & CO - Inotropes: dopaminergics e.g. dobutamine mainly increase HR/SV thus CO + contractility (may reduce SVR to cause vasodilatation)

Answer 51

Arterial line e.g. LIDCO or PICCO Transoesophageal doppler CVP monitoring

Answer 52

Cortisol Increased glucagon (decreased insulin) Renin Aldosterone -> stimulates reuptake of Na by acting on receptors between DCT + CD ADH/vasopressin -> produced in hypothalamus, stored/released from post. pituitary due to reduced volume, increased plasma osmolarity & angiotensin II acting to increase water uptake by CD via aquaporin insertion + NaCl reabsorption in thick ascending limb of LoH increasing interstitial concentration around loop enhancing ability to reabsorb water due to high osmotic gradient = concentrated small volume urine

Answer 53

Made up of LoH & vasa recta 1. Descending limb only permeable to water so water moves across tubular wall to medullary space so filtrate is now hypertonic 2. At thick ascending loop, Na transported out but water cannot move so water is drawn from descending limb into hyperosmolar medullary space both with aim to make filtrate hypertonic 3. Osmotic gradient multiplied between tubular fluid & interstitial space meaning urine is concentrated over short space along nephron with minimal energy expenditure

Answer 54

1. Kidneys sense BP decrease + release renin from JGA 2. Angiotensinogen is then released from the liver 3. This is converted to angiotensin I by renin 4. ACE in the lungs converts this into angiotensin II 5. Angiotensin II has a variety of effects all aiming to increase BP: - Arteriolar constriction - Enhances aldosterone secretion -> reabsorption of Na and water - Increase Na reabsorption thus water - Facilitates NA release by acting on postganglionic sympathetic neurons - Contraction of mesangial cells decreases GFR - Decreases brains sensitivity to baroreflex - Increase water intake from brain - Increases secretion of ADH/ACTH

Answer 55

1. Patient demographics, chest radiograph in PA view & date 2. RIPE - equidistant clavicles, 6-8 anterior ribs, mid thoracic vertebrae end plates should be visible & should be adequately exposed 3. Airways - trachea 4. Breathing - lung fields 5. Cardiac - contour? cardiomegaly? 6. Diaphragm 7. Everything else e.g. bones, soft tissues & artefact

Answer 56

No P-waves and irregular rhythm on ECG (rate must be counted by QRS complexes x 10 on rhythm strip) Causes: sepsis, MI, hypothermia & thyrotoxicosis Mx: 1. Cardioversion: DC shock, 300mg Amiodorone, repeat shock followed by 900mg/24h 2. Anticoagulation: unfractionated heparin 70units/kg as bolus then 15 units/kg/h till APTT 40-60s - in long-term may use DOAC or warfarin

Answer 57

A core body temperature of 36 degrees or less under anaesthesia Measured orally, axillary, rectally or via TM Risk factors: - Major exposed surgery -> reduce length of time where possible + only expose whats necessary - Pre-operative hypothermia <36 -> dont induce until warmer - Massive blood transfusion -> warmed IV products - General + regional anaesthetic

Answer 58

1. Radiation: to other cold bodies compounded by vasodilatation from anaesthesia 2. Evaporation due to large open abdominal wound 3. Conduction to operating table + cold infusion fluids 4. Convection: warming of cool air around patient Compounded by blood loss, sepsis + massive blood transfusion (>50% blood replaced in 12-24h) potentially

Answer 59

CVS: arrythmias Haematological: coagulopathy Neurological: reduced cerebral blood flow causing coma Renal: decreased renal blood flow + GFR

Answer 60

A pathological consumptive coagulopathy whereby concurrent coagulation & fibrinolysis occurs meaning microthrombi are formed, consume all the clotting factors and platelets leading to haemorrhage - occurs due to tissue injury/sepsis releasing tissue factor Characterised by thrombocytopenia, decreased fibrinogen & increased FDP Caused by: haemorrhage, sepsis, massive blood transfusion & hypothermia Mx: - FFP, cryoprecipitate, platelets (5 day shelf life) - Correct cause e.g. warm patient if hypothermic - TXA if bleeding - Involve haematologists

Answer 61

1. Vasoconstriction due to SM contraction by local reflexes, TXA2 + 5HT from activated platelets (impaired if vessel damaged) 2. Platelet aggregation to form plug (impaired in thrombocytopaenia/haemodilution) 3. Coagulation: intrinsic/extrinsic -> fibrinogen -> fibrin (also impaired by haemodilution)

Answer 62

Cell salvage/autologous transfusion to reinfuse patients own cells back into them Hypotensive technique Good haemostasis

Answer 63

Hypothermia Coagulopathy as stored blood lacks factors V + VIII TRALI Electrolyte imbalances e.g. hyperkalaemia

Answer 64

Continued haemorrhage Limb ischaemia Abdominal compartment syndrome Bowel ischaemia Organ failure

Answer 65

Failed venous access Needs long term medication Needs agents that cannot be given peripherally e.g. inotropes TPN Haemodialysis Complications: Immediate - pneumothorax, haemorrhage from artery, failed placement & arrythmia Late - infection, blockage, dislodgement & catheter #

Answer 66

Patient is being stepped down/discharged Infection No longer needs cardiac support Resolution of acute problem Remove it HEAD DOWN to prevent air embolism

Answer 67

IJV Subclavian Femoral PICC

Answer 68

Physical: congested neck veins, facial puffiness, lung creps + confusion Radiological: alveolar oedema, kerley B lines, cardiomegaly, upper lobe diversion & effusions

Answer 69

Tachycardia = reduced diastole time ->decreases cardiac filling -> increased cardiac load = MI Physiological stress response releases glucocorticoids & mineralocorticoids -> salt/water retention + ADH release stimulated + congestive HF reduces renal perfusion

Answer 70

Na+: 1-2meq/kg K+: 0.5-1meq/kg 150mmol/L Na in NaCl 131mmol/L Na in Hartmans

Answer 71

Mx: CCRISP A-E - stop IVF Fluid restrict O2 Furosemide Morphine (preload reduction) ACE-i (afterload reduction) Get ABG/CXR/ECG/bloods Liase with ITU as may need CPAP or inotropes (Dobutamine ideally) Prevention: CVP line to monitor Monitor UOP - strict IP/OP Report to hospital incident system if Dr induced + train juniors better

Answer 72

1. Bicarbonate (70%) 2. Carbaminohaemoglobin 3. Dissolved Equation: H2O + CO2 -> H2CO3 -> H+ (binds to Hb) + HCO3- (diffuses out to plasma) As HCO3- moves out, Cl- diffuses in to maintain balance (chloride shift)

Answer 73

Compensation occurs in 2 stages: 1. Acutely cellular buffering occurs (mins-hrs) elevating HCO3- only slightly 2. Renal compensation (3-5 days) so carbonic acid is excreted & HCO3- reabsorption increased

Answer 74

Type 1: hypoxaemia due to VQ mismatch Causes: pneumonia, bronchitis, PE & pneumothorax Type 2: hypoxaemia + hypercarbia caused by inadequate alveolar ventilation Causes: COPD, NMDs, reducing breathing effort due to drugs e.g. opioids & kyphoscholiosis -> elevation of CO2 causes central acidosis which stimulates central chemoreceptors increasing RR to blow off CO2

Answer 75

A-E as per CCRISP Humidified O2 Manage underlying cause e.g. Naloxone* if morphine Ventilation (non-invasive/invasive) ITU admission to considered if multi-organ support is required e.g. resp (ventilation), renal (haemodialysis), cardiac (inotropes) & neurological (ICP monitoring) *dose = 0.4-2mg IV initially repeating every 2-3 mins to max of 10mg SE: N&V, sweating, tachycardia & abdo cramps

Thorax Flashcards

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