Causes of chest pain Flashcards
Common causes of chest pain
Cardiovascular: cardiac ischaemia, pericarditis, aortic dissection
Respiratory: infection, pulmonary embolism
GI: GORD, oesophageal spasm, gastritis
MSK: trauma, costochondritis, intercostal nerve compression
How can you begin to distinguish which system is causing chest pain?
Aggravating factors cardiac - pain on exertion respiratory - on breathing GI - after meals MSK - moving and twisting
What is the presentation of stable angina?
Substernal, crushing central chest pain on exertion. May radiate to the arm, neck or jaw.
Lasts 2-10 minutes
Patients may have hypertension, prominent apex beat, aortic stenosis (ejection systolic murmur)
Describe how coronary atherosclerosis develops
Endothelial dysfention increasesits permeability. Lipids accumulate in subintimal spaces which are taken up by macrophages at focal sites, transforming them into foam cells.
Lesions produce fatty streaks on the endothelium of the artery.
The release of inflammatory cytokines from mactophages promotes further accumulation of macrophages. Smooth muscle and fibroblasts migrate and proliferate.
Smooth muscle sepatates lipid from enfothelium and fibrous cap forms over the lipid surface.
How can thrombus formation on atherosclerotic plaques occur?
Endothelial injury removes the endothelial covering the the plaque. Connective tissue matrix is exposed which activates platelets. Thrombus forms and adheres to the surface of the plaque
Plaque can can tear (ulcerate or rupture). Lipids are highly thrombogenic and cause platelt activation and thrombus formation within the plaque, expanding its volume and distorting its shape.
This can further occlude the lumen, eventually completely occluding the artery to cause ischaemia.
Unstable angina
Central heavy, crushing chest pain radiating to the jaw, neck or left arm.
Onset of < 1 month worsening andina or angina at rest.
What happens to the activity of the heart during/following an MI?
MI causes reduced contractility of the infarcted area (hypokinesia, akinesia, dyskinesia) which reduces SV, cardiav output and blood pressure.
Increased contractility of the non-infarcted area by haemodynamic changes (increased filling pressure, increased NorA and activation of Renin-AA) This causes tachycardia, vasoconstriction and sweating.
Longer term changes include ventricular dilation because tissue necrosis compromises the integrity of the ventricular wall (dead tissue replaced by rigid fibrous tissue). There is further reduction in SV
Signs of myocardial infarction
Pale, sweaty, in pain
Thready low volume pulse, usually fast
High/low bp
Breathless, third heart sound (signs of LV failure)
Bloods: raised creatine kinase and troponin T
Why is it important to differentiate between ST and non ST elevated MI?
Treatment differs.
STEMI is an emergency and requires angioplasty or thrombolysis because vessel is completely occluded
NSTEMI due to partial occlusion, require aggressive anti-platelets and angioplasty at
Symptoms of pericarditis
Sharp central chest pain (pleuretic)
Worse on deep breath, lying flat
Relieved by sitting forward
May follow viral infection (pyrexial)
Pericardial rub on auscultation
Presentation of aortic dissection
Sudden onset of excruciating chest pain, usually at the anterior chest radiating to the back between the scapula moving downward. Constant tearing pain, no precipitating/relieving factors
Can also present as cardiac tamponade, MI,
neurological symptoms due to loss of supply to spinal cord, renal failure, acute lower limb/visceral ischemia
Pathophysiology of aortic dissection
Occurs when a tear occurs in the intima of the aorta and it peels away forming two channels. (Blood may re-enter the main vessel wall distally)
Dissection can rupture through the adventitia and haemorrhage into adacent spaces (pericardium, pleural/peritoneal cavity).
Types of aortic dissection
A: Proximal lesions that involve the ascending aorta (more severe)
B: Distal lesions not involving ascending aorta
Management of aortic dissection
Diagnosis confirmed with CXR, CT, transoeophageal Echocardiogram
Urgent anti-hypertensive medication
type A: arch replacement
type B: stent
What causes unstable angina?
Transient blockage of a coronary artery by a thrombus that has formed at the site of an atheromatous plaque.
There is anginal pain at rest and the ECG shows ST segment depression or elevation.
Surgical interventions to improve coronary flow
Percutaneous transluminal coronary angioplasty (PTCA): which involves dilating the artery with a balloon catheter.
Stents: these are thin wire mesh structures that act as a permanent lining to keep the artery open. Stenting may be used in combination with PTCA.
Coronary artery bypass grafting (CABG): this is an operation in which the diseased artery is replaced with a short piece of vessel, such as a piece of the great saphenous vein in the leg, or a piece of the internal mammary artery.
Acute coronary syndromes
STEMI
NSTEMI
Unstable angina
All caused by rupture or erosion of the fibrous cap of a coronary artery plaque. This leads to platelet aggregation and adhesion, localized thrombosis, vasoconstriction and emboli resulting in reduced blood flow and myocardial ischemia.
Longer term changes in the heart following MI
Slippage of necrotic myocytes
Expansion of infarct zone
Ventricular dilatation
Further reduction in stroke volume
Pathophysiology of MI
MI: irreversible damage and necrosis of myocardial tissue due to prolonged ischemia and hypoxia.
Damaged tissue can precipitate abnormal cardiac rhythm and conduction blocks that impair contractility
Results in reduced cardiac output, stroke volume and blood pressure.
This elicits baroreceptor and neurohormonal reflexes to maintain cardiac output, however the increase in myocardial demand can precipitate ischemia and arrythmia - weakened structure of the myocardium causes ventricles to dilate and infarcted zone enlarges
Signs of pericarditis
Patient in pain, particularly when breathing
Pyrexial
Pericardial rub on auscultation
