Chest pain differentials and pathophysiology Flashcards
Chest pain differentials
-ACS
-PE
-MSK
-rTAA
-AKI
-pneumonia
-trauma
-costochondritis- inflammation where ribs join sternum, causing sharp pain when breathing or moving
-cocaine toxicity- occurs minutes to hours after cocaine use
ACS presentations
-chest pain- pressure, tightness
-radiating arm, jaw, neck, back
-SOB
-diaphoresis
-N+V
-dizziness, syncope
ACS pathophysiology
-atherosclerosis or plaque forms in coronary arteries
-plaque ruptures exposing thrombogenic lipid core
-this causes platelet activation causing vasoconstriction and triggers clotting cascade
-this leads to conversion of fibrinogen into insoluble fibrin forming thrombus
-partial occlusion= UA or NSTEMI
-complete occlusion- STEMI
PE presentations
-sudden onset dyspnoea
-pleuritic chest pain
-haemoptysis (cough blood)
-tachypnoea
-tachycardia
-signs DVT
-syncope
Severe
-jugular vein distension
-hypotension
PE pathophysiology
-commonly originates from DVT
-the DVT clot breaks away forming an embolus
-travels through inferior vena cava, R atria, R ventricle to pulmonary arteries
-large emboli block pulmonary arteries increasing pulmonary resistance
-leads to lack of oxygenated blood and some blood backflowing into R ventricle
MSK presentations
-localized pain, one sided
-sharp, aching or burning
-worse with movement, deep breathing or palpation
-crepitus
-better with rest, NSAIDS
eg. costochondritis (inflammation of costal cartilage)
rTAA pathophysiology
-due to chronic HTN, atherosclerosis, connective tissue disorders eg. marfan
-over time weakened area dilates forming aneurysm
-wall continues to weaken causing intima and media layers to tear = dissection
- when the outer layer fails, rupture occurs leading to massive internal bleeding
rTAA presentations
-severe sudden onset chest, upper back pain (tearing, ripping)
-radiates to back, shoulders, abdo
-syncope, altered mental status
-cold, clammy
-SOB
-pulsatile mass
Pneumonia pathophysiology
-infection of the alveoli and lung parenchyma
-caused by bacteria, viruses, or fungi
-triggers an inflammatory response, leading to:
1.Alveolar inflammation – The alveoli fill with exudate, pus, and immune cells, impairing gas exchange.
2.Vascular permeability increases, causing fluid to leak into the alveoli, leading to crackles on auscultation.
3.Hypoxia – Reduced oxygen exchange can cause low SpO₂ and increased respiratory effort.
4.Systemic response – The infection triggers a fever, tachycardia, and increased WBC count as the immune system fights off the pathogen.
Pneumonia presentations
-fever
-productive cough
-pleuritic chest pain
-dyspnoea, tachypnoea
-crackles on auscultation
-hypo resonance on percussion
Cocaine toxicity pathophysiology
-blocks reuptake of noradrenaline, dopamine and serotonin
-causes excessive sympathetic stimulation -> HTN, tachycardia, vasoconstriction
-increased myocardial O2 demand
Cocaine toxicity presentations
-chest pain, acute MI
-HTN
-ventricular arrythmias
-seizures, stroke
-delirium
-hyperthermia
AKI presentations
-decreased urine
-peripheral oedema
-SOB
-fatigue
-confusion/ altered mental state
-N+V
-CP/ pressure if fluid accumulates around heart
AKI pathophysiology
Prerenal AKI
-decreased blood flow, less blood in glomerulus, lower GFR, activates renin angiotensin aldosterone system which causes more Na+, urea and water reabsorption
Intrarenal
-decrease blood flow to kidney cells, not enough oxygen so ischaemic then necrotic, dead cell matter blocks tubule, increasing pressure within tubule, decreasing GFR
Postrenal
-obstruction to outflow vessels due to kidney stones, abdo tumour, build up of urine, increase pressure within tubule, decrease GFR
