Learning Objective Flashcards
What are the three common mechanisms of chest pain?
Ischaemia - MI, PE causing pleurisy, pain in diffuse oesophageal spasm
Inflammation - pleuritis, pericarditis, oesophagitis, aortitis
Mechanical trauma - aortic dissection, traumatic chest wall injury, pneumothorax, Mallory-Weiss tear
Describe the typical clinical syndromes of chest pain and indicate their pathological and anatomical basis.
Ischaemia - inadequate myocardial perfusion (anaerobic metabolism –> lactic acid –> nociceptor activation); retrosternal chest pain, radiation (L) arm, jaw, epigastrium; exacerbated by exertion (exercise, motion, eating); relieved by rest, nitrates, associated with SOC, pale/diaphoretic
Pleuritic - inflammation of mesothelial surfaces rubbing (pleuritis - PE, pneumonia, pneumo/haemothorax; pericarditis; sub-diaphragmatic irritation); sharp, stabbing pain; localised over region of inflammation, exacerbated by deep inspiration (“catches” the pt); pericarditis pain relieved by sitting up, leaning forward; pericarditis causes - viral (coxsachie, echo), idiopathic, malignancy (lung, breast, bone), bacterial (pneumoniae, TB), post-MI, autoimmune (dressler’s, SLE, RA)
Chest wall - multiple pathologies (rib fracture, arthritis, intercostal m injury, costochondritis); variable, often related to manual work/sport; local tenderness over rib/costal cartilage, spinal pain often perceived to radiate foward from back, may vary with posture/movement of upper body
Vascular - aortic dissection; sudden, tearing chest pain radiating to back; associated features paraesthesiae, anaesthesiae, weakness
Radicular - spinal nerve root inflammation or compression (viral; traumatic - disc herniation/fracture; degenerative - arthritis); stabbing pain in a dermatomal distribution, associated paraesthesiae, anaesthesiae, weakness
Psychological - anxiety (neurotic personality, emotional stressors); atypia (pain not characteristic of defineable syndrome); assocaited hyperventilation may be present
Oesophageal - oesophagitis due to gastro-oesophageal reflux disease/oesophageal spasm; burning/scalding pain radiating from epigastrium; exacerbated by bending forward, eating, lying down; associated water brash, relieved by antacid
Referred - usually from epigastrium (cholecystitis, pancreatitis, hepatitis); may mimic chest pain
Massive PE: severe, sudden retrosternal pain with rapid haemodynamic collapse, dyspnoea, cyanosis
Bronchospasm: chest tightness during asthmatic attack may be difficult to distinguish from ischaemia, associated wheeze
Discuss the epidemiology of CHD and its associated morbidity and mortality.
IHD = most common cause of CV morbidity and mortality in Aus
80% of all cardiac deaths; atherosclerosis and thromboembolism msot common
Coronary heart disease is the most common cause of death (20%)
IHD incidence increases with age –> peak incidence symptomatic IHD is 50-60 for me and 60-70 for women
M:F 2:1 overall however 8:1 if aged 70
40% decrease in CV mortality in last 10 years - modification of lifestyle factors, therapeutic advances (early detection and intervention, mx of HTN, DM, dyslipidaemia)
Outline the common sites of coronary artery atherosclerosis.
Left anterior descending: major branches are the septal perforating branch and diagonal branches; it follows the anterior interventricular groove and supplies the anterolateral wall of the left ventricle, anterior 2/3 interventricular septum. Atherosclerosis usually occurs in the first 2cm and it causes an anterior or anterolateral infarct
Left circumflex artery: major branches are the marginal branches, anastomosis with the RCA at the junction of the R and L atria; runs along the L atrioventricular groove and supplies to lateral wall of the left ventricle and left atriu. Atherosclerosis occurs in the proximal and/or distal 1/3 and causes a lateral infarct.
Right coronary artery: major branches are the marginal branches and the posterior descending and atrioventricular nodal arteries (in 90% of people, 10% have the latter two off the LCA); runs along the atrial appendage and pulmonary trunk then within the right atrioventricular groove and supplies the inferior/posterior LV wall, posterior 1/3 IVS, posterior wall of the RV and the RA. Atherosclerosis occurs in the first 2cm and causes a posterior or inferior infarct.
Describe the relationship between the complications of atherosclerosis and the clinical syndromes of stable and unstable angina.
Stable angina: fixed, stabl, occluxive plaque, symptomatic at >75% stenosis, basal myocardial oxygen is adequate but inefficient during exercise; predictable, exertional ischaemic chest pain, 15 minutes, may progress to myocardial infarction
Variant angina: arterial spasm usually in the setting of some pre-existing atherosclerosis; chest pain at rest which may be difficult to distinguish clinically from unstable angina; prompt response usually to nitrates, calcium channel blockers
What are three major exacerbating factors in ischaemic chest pain?
Harmful stress response to ischaemia (profound increased sympathetic tone and endocrine [adrenalin] response) - vasospasm, tachycardia (reduced duration of diastole - when coronary artery filling occurs)
Pre-existing impaired myocardial oxygen supply - anaemic, hypoxaemia (pulmonary - COPD; cardiac - R-L shunting)
Pre-existing increased myocardial oxygen demand - myocardial hypertrophy (secondary to HTN, aortic stenosis), hyperthyroidism (increased contractility, increased HR)
Relate changes in the myocardium to the ECG abnormalities that characterise myocardial infarction.
Anterolateral (LAD): I, aVL, V3-V6
Lateral (LCx): I, aVL, V5-V6
Inferior (RCA): II, III, aVF
ST elevation MI: typically indicates transmural infarction
Non-ST elevation MI: typically indicates subendothelial infarction (most susceptible to ischaemia because it is most distal in the coronary arterial tree)
Isolated ST depression: indicates ischaemia only –> may occur during stable angina –> in the absence of other progressive changes does not indicate infarct
Evolution of ECG changes:
Minutes - variable ST changes, hyperacute “peaked” T waves; ST depression may indicate early ischaemia, ST elevation indicates more severe occlusion
Hours - ST elevation, T wave inversion
Days - persistent T wave inverrsion, ST segment returned to baseline
Weeks - pathological Q waves which persist indefinitely
Describe the way in which estimation of blood enzyme and protein levels may aid in the diagnosis of myocardial infarction. In particular, outline the time course of changes in serum levels of cardiac troponins following myocardial infarction.
Troponin T and I - released w/in 4-6h of damage, peaks at 24-36h, remain elevated for 2 weeks; most sensitive marker of myocardial damage
CK-MB - released w/in 4-6h of damage, peaks at 12h, remains elevated for 48-72h; helpful to diagnose re–infarction (serial enzyme measurements - 8 hrly) but persistent elevation may indicate more chronic state (sepsis, renal disease)
Biochemical changes:
Acute phase reactants - leukocytosis, acute phase response proteins elevated (fibrinogen, gamma globulin, CRP, ESR)
Sensitive biomarkers - creatinine kinase (may indicate myocardial or skeletal damage), AST (peak 48h) and LDH (peak 72h) are both sensitive but not specific
What pharmacological treatments are used to limit the extent of myocardial infarction and what is their mechanism of action?
Antiplatelets:
Aspirin (300mg stat, then 100mg daily) - non-selective COX inhibition prevents thromboxane A2 synthesis to stop aggregation; can cause GIT irritation/ulceration, blood loss; contraindicated if active bleeding or hypersensitivity
Clopidogrel (300mg stat, then 75mg daily with aspirin) - inhibition of ADP to prevent platelet activation; can cause bleeding, rarely TTP, aplastic anaemia; contraindicated if active bleeding or hypersensitivity
Vasodilators: Glyceryl trinitrate (GTN - anginine; up to 1500ug 3 tablets sublingual, prior to IV) - vasodilation (smooth muscle relaxation), platelet inhibition; can cause flushing, orthostatic hypotension, reflex tachycardia, fluid retention; contraindicated in hypotensive conditions, head injury, cerebral haemorrhage, severe anaemia
Anticoagulants:
Heparin (5000IU bolus + infusion 1000IU/hr) - binds and activates antithrombin III –> increased proteolysis of coagulation factors (II, IX, X, XI, XII); can cause bleeding/bruising, hyperkalaemia, mild thrombocytopenia, rarely HIT: contraindicated is severe thrombocytopenia, uncontrolled active bleeding (except when due to DIC), reverse with protamine, FFP or cryoprecipitate
Thrombolytics:
Alteplase (tPA - 15mg bolus then 0.75mg/kg over 30m, then 0.5mg/kg over 60m) - activates plasminogen to plasmin (fibrinolysis); can cause severe bleeding including GIT haemorrhage and/or intracranial haemorrhage; contraindicated if active bleeding, recent major surgery/trauma, hx of haemorrhagic stroke ever, TIA last 12 months, AV malformation, careful in severe HTN and pregnancy; reverse with tranexamic acid
Streptokinase - uncommonly used today due to poor clot specificity (also reduces circulating fibrinogen) and immunogenic effects (may induce allergic reaction)
Discuss the common causes, typical pathological changes and the clinical consequences of aortic dissection.
Definition: a condition in which blood accumulates between the intima and media of the aorta, creating a false lumen.
Aetiology: >80% due to hypertension; collagen disorders (eg. Marfan’s syndrome); trauma due to injury, aortic surgery, cardiac catheterisation; 3rd trimester pregnancy, aortic coarctation, aortic aneurysm, fibromuscular dysplasia, aortic atherosclerosis
Pathology: cystic medial degeneration; Type A involves aortic arch, Type B involves the decending aorta only
Clinical features: sudden, tearing pain in anterior chest radiating to back; asymmetry of brachial, carotid and/or femoral pulses, hypertension unless frank rupture; dissection may compress aortic branches (MI, stroke, paraplegia, acute abdomen, ARF, acute limb ischaemia), rupture into pericardium, pleura or peritoneuma or can cause retrograde dissection into the aortic root (aortic regurgitation)
List the causes of pericarditis, and outline the clinical features and potential complications of this condition.
Aetiology: complication of acute MI, viral; uraemia, malignant disease, trauma, CT disease, bacterial infection, TB infection, rheumatic fever
Clinical features: pericardial pain (retrosternal, radiates to shoulders/neck, aggravated by deep breathing/movement, relieved by sitting forward); pericardial friction rub (high pitched scratching noise, loudest in systole but may also be audible in diastole); low grade fever, widespread ST elevation with upward concavity of ECG, PR depression, no Q waves
Complications: pericardial effusion, cardiac tamponade (increased JVP, hypotension, pulsus parodoxus, oliguria), chronic obstructive pericarditis causing heart failure
Describe the natural hx of an atherosclerotic plaque, and the diverse physiological and clinical consequences that may arise from a complicated lesion.
Ath. is a disease of large and medium sized arteries, characterised by focal or eccentric thickening of the intima due to inflammatory and fibrotic lesions (associated with lipid deposition).
Fatty streaks (1mm) - foam cells Early fibro-fatty plaques - fibrous cap with variably large lipid core (3-15mm); chronic inflammatory cells prominent at edge of plaque, fibrosis (cellular proliferation, fibrous matrix secretion); advanced plaques - intimal thickening with atrophy of underlying media and calcification; get vascular stenosis due to luminal protrusion and calcification causing poor vessel compliance, aneurysmal dilatation due to medial atrophy and predisposing to mural thrombi; complicated lesion - due to palque rupture from mechanical bulging by lipid core, inflammatory cell degradative enzymes, intraluminal thrombosis +/- distal embolisation, choelsterol embolisation, intraplaque haemorrhage
Complcations: chronic tissue ischaemia due to progressive vascular stenosis; acute tissue ischaemia due to thromboembolic phenomena superimposed on complicated plaque, aneurysmal rupture due to medial weakening
Describe the classification of aneurysms.
Saccular: least common, usually related to heritable factors, invovle part of circumference only
Fusiform: most common, involve entire circumference of vessel wall, may be very large
