Hemostasis
Platelet Functions
Reduce blood loss via. vasoconstrictors; promote clotting; attract neutrophils/monocytes
Fibrinolysis
Dissolution of a clot. Factor 12 leads to Kallikrein enzyme, which turns plasminogen to plasmin, dissolving fibrin.
Role of Pericardium
Allows heart beat w/out friction, gives room for heart to expand.
Intercalated Discs
Join cardiomyocytes with interdigitating folds, mechanical, and electrical junctions.
Depolarization Phase
Sodium gates open, Na+ rushes quick, peaks at +30 mV and closes
Production of Platelets
Thrombopoiesis, Megakaryoblasts, Megakaryocytes, Platelets
Natural Anticoagulants
Heparin interferes with prothrombin activator. Antithrombin (from liver) deactivates thrombin before it can work on fibrinogen.
Ventricular Diastole
Blood in the aorta surges toward the heart and into the openings of the coronary artery
Interdigitating Folds
Plateau Phase
Ca++ voltage gates open and trigger the sarcoplasmic reticulum. Ca++ binds to troponin, triggering contraction
Vascular Spasm
Prompt constriction of broken vessel; caused by nociceptors and vasoconstrictors released by platelets (serotonin)
Myeloblasts; Monoblasts; Lymphoblasts
Neutrophils, eosinophils, basophils; Monocytes; Lymphocytes
What does the Right Coronary Artery Supply?
The right atrium and the SA node
Desmosomes (tight junctions)
Mechanical linkages that prevent contracting cardiomyocytes from being pulled apart from each other.
Repolarization Phase
Ca++ channels close, K+ channels open and returns to resting potential. Refractory per. of 250ms.
Platelet Plug
Platelet pseudopods stick to damaged vessel, form a platelet plug and platelets degranulate.
Gallbladder Bile Formation
Iron is removed from heme, heme's pigment turns into biliverden, converts to bilirubin, which the liver removes and secretes into bile.
Angina Pectoris
Chest pain from partial blockage of coronary blood flow. Myocardium shifts to anaerobic respiration, lactate causes pain.
Electrical (GAP) Junctions
Allow ions to flow between cells; can stimulate neighbors. Entire myocardium acts like a unified cell
Cardiomyocyte Resting Potential
-90mV. SA node has no stable resting potential, but starts at -60 mV, leaky Na+
Coagulation
Factor X leads to prothrombin A, which converts prothrombin to thrombin, which converts fibrinogen to fibrin, to form clot.
Branches of the Coronary Sinus
Great cardiac vein, posterior interventricular, and left marginal veins.
Myocardial Infarction
Death of a myocardium patch, resulting from long term blockage of coronary circulation
Cardiac Muscle
Rich in myoglobin and glycogen, if fuel is not present it can adapt to fatty acids.
Sinus Rhythm
Normal heartbeat triggered by SA node. 70-80BPM (vagal tone). SA node normally fires every 0.8 seconds