Angina – Chest Pain – Part 5
A 69 year old male presents to the emergency room complaining of increasingly severe chest pain for the past 2 hours. He has a 45 pack year history of cigarette smoking. Medications include thiazide, captopril and atorvastatin.
- Describe the patient.
- What is the chief complaint and differential diagnosis?
- Describe the blood supply of the heart.
- Normal structure and local regulation
- Ischemia (supply vs demand)
- Describe types of plaque
- Stable plaque (& CPC)
- Unstable plaque (& CPC)
- Describe the clinical-pathologic correlation:
- What next?
- EKG results:
- What is the interpretation and next action? (3)
- Describe the natural history for an acute STEMI (CPC)
- How should the patient be treated?
- Acute inflammation
Clinical pathologic correlation: systemic effects
- When an acute infection becomes severe enough, the local production of cytokines and hormones gets into the systemic circulation and causes generalized responses, typically called sepsis. Sepsis is a systemic inflammatory response syndrome (SIRS) due to infection.
- IL-1 and fever:
· Fever is an increase in core temperature due to the hypothalamus elevating the body’s set point. Endothelial cell overlying the hypothalamic temperature centers have an IL-1 receptor. When stimulated by a cytokine like IL-1, called a pyrogen, the endothelial cells release PGE2 that crosses the blood brain barrier and stimulates the hypothalamic temperature regulatory neurons.
· The commonest therapy for fever is a NSAID. The Cox inhibition decreases PGE2 production.
- IL-6 and the acute phase reactants (APRs):
· Hepatocytes have an IL-6 receptor that triggers the production of over 30 proteins as part of a systemic response to inflammation. An APR is any protein or cell that increases or decreases more than 20% in inflammation. APRs are used in clinical medicine to assess the degree of inflammation. Examples include C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) which is determined mostly by fibrinogen.
- TNF-α and shock:
· High levels of cytokines can cause dysregulation of endothelial cells. Endothelial cells are key regulators of peripheral resistance (TPR) and their dysfunction can lead to a loss of TPR and blood pressure. Shock is defined as blood pressure is < 90 mmHg systolic pressure and leads to ineffective perfusion. Septic shock is a type of distributive shock.
- Massive mast cell degranulation, seen with IgE allergic reactions such as peanut or bee sting allergies can lead to shock from vasodilation and fluid extravasation. It is a type of distributive shock as it is due to vasomotor collapse.
Natural history of STEMI
General pathology: gross patterns of necrosis