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59 Cards in this Set
- Front
- Back
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Causes of pleural effusions |
1/ transudate <30g/L
- cardiac failure - hypoalbuminaemia (nephrotic syndrome, chronic liver disease) 2/ exudate - TB - inflammatory - malignant - pancreatitis - radiation 3/ haemothorax 4/ chylothorax |
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signs of pleural effusion
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- trachea deviated away from massive effusion
- reduced chest expansion on affected side - stony dull percussion note - reduced vocal femoritus/vocal resonance - breath sounds reduced over effusion, bronchial breath sounds above |
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pulmonary fibrosis pathology
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- initial inflammatory reaction impairs gas exchange followed by collagen deposition and fibrosis
- leads to small lungs with reduced compliance |
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Causes of pulmonary fibrosis (upper lobe)
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SSCHAART
- silicosis - sarcoidosis - coal workers pneumoconiosis - ankylosing spondylitis - radiation - tuberculosis |
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causes of pulmonary fibrosis (lower lobe)
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RASCO
- rheumatoid arthritis - asbestosis - scleroderma - cryptogenic fibrosing alvelolitis - other eg drugs (methotrexate, amiodarone, bleomycin) |
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sarcoidosis
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- systemic disease with non-caseating granulomas which occur throughout body and heal via fibrosis
- pulmonary changes in 50%, typically hilar lymphadenopathy - R heart failure possible due to lung disease - cardiac conduction defects |
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pulmonary HTN (defn and causes)
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- defined as mean PAP >25mmHg |
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signs of pulmonary HTN
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- general: tachyopnoea, cyanosis |
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bronchiectasis
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- chronic dilation of airways leading to impaired clearance of mucus and chronic infection
- causes congenital eg cilary dysfunction, cyctic fibrosis acquired eg whooping cough, pneumonia, foreign body |
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pulsus paradoxus
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- fall of >20mmHg on inspiration
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signs of severe asthma
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- physical exhaustion
- only able to talk in words - silent chest - SpO2 <90% - HR >120bpm - PEFR <50% |
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asthma
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- reversible chronic airflow obstruction due to constriction of smooth muscle in the airways, inflammation and hypersecretion of mucus
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COPD
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- spectrum of abnormalities from emphysema to bronchitis
- emphysema is dilation and destruction of airways beyond terminal bronchioles - chronic bronchitis mucus gland hypertrophy and hypersecretion of mucus leading to chronic cough - bronchitis requires daily production of mucus for 3/12 in 2 consecutive yeas |
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AR signs, signs severe and causes
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- waterhammer pulse
- prominent carotid pulsations (corrigan's sign) - displaced and hyperkinetic apex beat - thrill if lean forward in full expiration - early decrescendo diastolic murmur - may be associated with Austin Flint due to backward jet disturbing mitral valve severe disease: - collapsing pulse - wide pulse pressure - LV S3 causes: - connective tissue disease eg marfans - ankylosing spondylitis - rheumatic - congenital - aortic root dilation |
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AR intra-op goals
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intra-op goals
- high normal HR - low SVR - maintain contractility |
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Aortic valve area and gradients with AS
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normal is >2.6-3.5m
mild 1.6-2.5cm and mean gradient <25mmHg moderate 1-1.5cm and mean gradient 25-40mmHg severe <1cm and mean gradient >40mmHg critical <0.6cm and mean gradient >50mmHg |
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AS pathophysiology
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causes
- sclerosis (most common) - bicuspid - rheumatic (rare) -LVOT obstruction leads to LVH leads to diastolic dysfunction - diastolic dysfunction of LV leads to greater reliance on atrial systole to contribute to LVEDV (~40% cf 15%) - increased O2 demand |
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AS classic symptoms
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- exertional dyspnoea
- exertional syncope - angina |
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AS signs
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- slow rising and low volume pulse
- apex beat hyperdynamic, slightly displaced - ejection systolic murmur radiating to carotids, with possible reversed splitting (normal splitting is AV closes before PV) - murmur loudest when sitting up in full expiration Ix - ECG: LVH with strain - CXR: poststernotic root dilation |
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AS signs severe disease
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- palpable thrill
- LVF - weak carotid pulse - plateau pulse |
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AS intraop management goals
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- maintain preload
- maintain low normal HR in SR - contractility normal/elevated - keep afterload up to allow for coronary perfusion |
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LVH and RVH criteria on ECG
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- LVH has sum of V1 S wave and large of R wave in V5 or V6 being greater than 35mm or 7 squares
- RVH has R wave >7mm in V1 |
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HOCM
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- autosomal dominant
- due to abnormal hypertrophy of ventricular muscle in septum or affecting LVOT or RVOT - can lead to LVOT obstruction in systole due to contraction of hypertrophied muscle. - can be further exacerbated by anterior leaflet of mitral valve getting caught in LVOT (SAM) - prone to arrhythmias and sudden cardiac death - on B blockers and PPM/ICD |
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HOCM symptoms and signs
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- report dyspnoea, angina, syncope, sudden death from arrhythmias and sudden increase in LVOT obstruction
Ex findings - sharp rising jerky pulse due to rapid ejection of blood followed by obstruction - JVP prominent a wave due to contraction of atria against stiff ventricle - double apical impulse due to forceful atrial contraction - auscultation late systolic murmur at Left sternal edge (mitral area) -S4 - murmur louder with valsalva and exercise, reduced with squatting (?increases afterload and decreases LVOT obstruction) |
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HOCM intraop goals
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- maintain SR and low HR
- maintain preload - low contractility (avoid inotropes, use B blockers) - high SVR |
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HTN causes
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1/ essential (95%)
2/ secondary - endocrine eg conns, phaeo, acromegaly - CVS eg coarctation aorta - renal eg renal artery stenosis, pyelonephritis, connective tissue disorder - other eg raised ICP (cushings sign) |
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HTN exam
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- look for rare secondary causes eg cushings, acromegaly
- look for signs of radio-femoral delay for coarctation - take BP lying and standing - examine fundi (flame haemorrhages) - S4 when BP >180/110 - palpate abdomen for abdominal masses eg adrenal tumour |
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HTN end organ damage
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- CNS: CVA, eye disease
- CVS: IHD, LVH, AAA, PVD - Renal: failure |
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Peri-op Rx HTN
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- AHA/ACC says cancel elective surgery if BP >180/110 and evidence of end organ disease and Ix
- in theatre keep MAP within 20% or normal |
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mitral valve sizes
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normal 4-6cm
symptom free until 1.5cm moderate 1-1.5cm severe <1cm |
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mitral stenosis pathology
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- LV underfills (generally unaffacted)
- LA dilates - increases risk of AF - chronically dilated LA leads to pulmonary HTN common cause is rheumatic heart disease - RV hypertrophies - can lead to TR |
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MS history
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- dyspnoea
- othopnoea and PND - haemoptysis - fatigue due to pulmonary HTN - with RHF ascites, ankle oedema |
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MS examination
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- inspection: tachyopnoea and mitral facies
- AF - JVP: prominent a wave if RVF present - tapping apex beat - RV heave if pulmonary HTN present - auscultation: snapping S1, loud S2 if pulmonary HTN present, low rumbling diastolic murmur |
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signs of severe MS
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- small volume pulse
- soft S1 - diastolic thrill - signs of pulmonary HTN |
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Intra-op management
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- maintain preload, avoid fluid excess as will lead to APO
- low HR in SR crucial (treat tachycardia aggressively) - high normal SVR (fixed output state may compromise coronary perfusion) - avoid factors which increase pulm HTN eg acidosis, hypoxia, hypercarbia |
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mitral regurgitation
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- regurgitant MV allows part of LV SV to regurgitate into the LA. Makes LV ejection fraction supranormal
- this places a volume load on both LA and LV - pulmonary vascular congestion develops followed by pulmonary HTN - degree of regurgitation depends on afterload, size of regurgitant orifice and HR |
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MR symptoms and signs
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Hx: dysnpnoea, fatigue and tachyopnoea
Ex - pulse sharp upstroke or normal. AF common - apex beat displaced, hyperdynamic. May feel pansystolic thrill - auscultation soft or absent S1. S3 due to rapid ventricular filling. Pansystolic murmur radiatingto axilla - severe disease can lead to pulmonary HTN |
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causes of MR
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- MVP
- degenerative with aging - rheumatic - papillary muscle dysfunction due to LV failure or ischaemia - cardiomyopathy - connective tissue disorder eg marfans |
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Ix for MR
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ECG: LA enlargement, AF
CXR: LA and LV enlargement |
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intraop goals for MR
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- maintain preload
- high HR - normal contractility - low SVR |
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Chronic liver disease causes
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- virus eg Hep B/C
- ETOH - drug - metabolic eg wilsons, haemochromatosis - other eg autoimmune hepatitis, PSC, venous outflow obstruction |
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Chronic liver disease complications
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- H and M
- encephalopathy (4 grades, caused by sedatives, high protein, H and M, infection, trauma, constipation) - ascites - hypoglycaemia - pancreatitis - pancytopaenia - renal failure |
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chronic liver disease signs
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inspection: jaundice, muscle wasting, encephalopathy, tattoos |
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Child-Pugh classification
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A - albumin
B - bilirubin C- clotting (INR) D - encephalopathy E - (e)ascites Child A - 5% mortality Child B - 25% mortality Child C - >50% mortality scores on 1, 2, 3 5-6 child pugh A 7-10 child pugh B >10 child pugh C |
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MELD
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- used as mortality prognostic tool to stratify liver transplant patients
- uses bilrubin, creatinine and INR |
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Parkinsons disease
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- due to degeneration of substantia nigra leads to deficiency in central dopamine
- look for lack of facial expression and flexed posture - gait: shuffling, difficult to start walking then difficultly in stopping - bradykinesia decrease in speed of complex tasks eg tapping fingers - resting pill rolling tremor - increase in tone - glabellar tap - monotonous voice and faint - weakness of upward gaze |
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Causes of peripheral neuropathy
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- ETOH abuse
- metabolic eg DM - vitamin deficiency eg B12 - drugs eg amiodarone, vincristine - paraneoplastic - guillian-barre syndrome - idiopathic - heriditary |
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upper motor vs lower motor neuron lesion
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upper motor (lesiona bove anterior horn eg motor pathways in cerebral cortex, internal capsule, brainstem or cord)):
- hypertonic - hyperreflexic - contraction of upper limb flexors and lower limb extensors (more powerful muscle groups) - all muscles weaker than normal Lower motor: - fasciculations - muscle wasting - hypotonic - hyporeflexic |
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upper limb myotomes
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shoulder ABduction: C5/6
shoulder adduction: C6/7/8 elbow flexion: C5/6 elbow extension: C7/8 wrist flexion/extension: C6/7 finger flexion and extension: C7/8 small muscles T1 |
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lower limb myotomes
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hip flexion: L2/3
hip extension: L5-S1/2 knee extension: L3/4 knee flexion: L5/S1 ankle dorsiflexion: L4/5 ankle plantarflexion: S1/2 |
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scleroderma
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- disorder of connective tissue
- CREST syndrome more localised form (calcinosus, raynauds, oesophageal dysmotility, scleradactyly, telangiectasia) - inspection: cachexia, skin tight, thickened and indurated, bird like facies - hands: calcinosus, raynauds, teleangiectasia - face: loss of normal skinfolds/wrinkles, unable to close eyes, reduced mouth opening - chest : pulmonary fibrosis or pleural effusion |
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cardiac tamponade
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-maintain preload
- SVR will be up, maintain - keep rate up as CO is HR dependent (Avoid bradycardia) - maintain contractility/increase - post correction, may have marked increase in BP, anticipate and deepen anaesthesia - avoid PPV as will cause decreased VR and bradycardia - can use SV technique until pericardial sac is opened or can put drain in under LA |
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hyperparathyroidism
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- primary from hyperplasia of gland
- secondary in renal failure due to prolonged hypocalcaemia - tertiary from prolonged secondary becomes self- secreting tumour symptoms of hyperparathyroidism related to hypercalcaemia CVS: shortened PR, prolonged Qt, CNS: psychosis, neuropathy Renal: stones and polyuria and polydipsia GIT: pain, nausea, pancreatitis |
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ECG changes with hypercalcaemia
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- prolonged PR
shortened Qt |
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ECG changes with hyperkalaemia
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- peaked T waves
- widening QRS - flattened P wave - ST depression - VF -asystole |
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ECG changes with hypokalaemia
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- T wave flattening and inversion
- prominent U wave - ST depression - prolonged PR |
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Acid base correction for acute and chronic resp acidosis
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- acute resp acidosis, HCO3 goes up by 1 for each 10mmHg CO2 above 40mmHg
- chronic resp acidosis, HCO3goes up by 4 for each 10mmHg CO2 above 40mmHg |
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acid base correction for acute and chronic metabolic alkalosis
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- acute alkalosis, CO2 = 1.5x HCO3 + 8
- chronic CO2 = 0.7xHCO3 + 20 |
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acid base correction for acute and chronic resp alkalosis
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- acute alkalosis HCO3 down by 2 for each CO2 10mmHg below 40mmHg
- chronic alkalosis HCO3 down by 5 for each 10mmHg below 40mmHg |
