CSB520 Lecture Notes - Lecture 7: Circumflex, Fibrin, Ascites
Week 6 Lecture - Cardiovascular Pathology
Friday, 15 April 2016 12:09 PM
3 Layers of the Heart:3 Layers of the Heart:
•Endocardium - inner flattened layer of cells (includes the valves)
•Myocardium - thickest layer, muscle
•Pericardium - outer layer, 2 membranes that glide over each other
HeartHeart
•4 contractile chambers
•Right side - pumping blood to lungs for reoxygenation
•Left side - pumping blood out to aorta into systemic circulation
•Movement of blood occurs in response to pressure gradients
○High to low pressure environments
•Direction of movement facilitated by valves
•Cardiac cycle:
○Atrial systole
○Atrial diastole
○Ventricular systole - first phase
•Ventricular contraction pushes AV valves close
○Ventricular systole - second phase
•Ventricular pressure rises and semilunar valves open and blood is ejected
○Ventricular diastole - early
•As ventricles relax, pressure in ventricles drop, blood flows back and forces
semilunar valves closed
•Blood flows into atria
○Ventricular diastole - late
•Ventricles fill passively
Physiology TermsPhysiology Terms
•Systole: Systole: when ventricles contract
•Diastole:Diastole: when ventricles relax
•CO:CO: amount of blood ejected from the ventricles every minute
○Indicates cardiac performance
○CO = HR x SV
•HR = HR = beats per minute
○Influenced by many factors, but most important:
•SNS vs PNS
•SVSV: depends on preload, after load & contractility of the heart
○Preload:Preload: volume/loading conditions after diastole related to blood volume &
venous return
•How much blood is coming back into the heart
○Afterload:Afterload: force required to eject blood out of the ventricles related to
resistance
•How much force is required to overcome the blood coming into the
ventricle
•Contractility:Contractility:
○Generated by actin-myosin cross-bridge formation
○Greater actin-myosin interaction = greater force generated
○Contractile force generates blood pressure
○If actin-myosin is lost (e.g. infarction or atrophy) - force of contraction is
decreased
○If actin-myosin is gained (hypertrophy) - increase force of contraction
HypertrophyHypertrophy
•Cells need their waste products to diffuse into the capillary bed and at the same time
get stuff from the capillary
•So if there's hypertrophy is going to be harder and can caused added stress
•Physiological vs Pathological Hypertrophy
○Physiological: athlete's heart - more uniform hypertrophy (lungs will be adding
to the stress as well)
•Cells would have more elastic fibres & antioxidants
•Increase of density in capillary beds
○Pathological: high BP, heart responds
•But we don't see changes in elasticity, no extra budding in capillary beds,
no increase of antioxidants
Ejection FractionEjection Fraction
•The % of blood pumped out of the ventricles w/ each contraction
•Normal = 65%
•Systolic dysfunction - impaired contractility --> decreased ejection fraction & CO
•Diastolic dysfunction --> Normal ejection fraction but impaired filling - decreased
preload, SV and CO
•Note that the ventricular dysfunction is not the same as heart failure BUT can LEAD to
heart failure
•Compensation means that CO is often normal @ rest
Blood for the HeartBlood for the Heart
•Ischaemic heart disease - atherosclerosis in the coronary arteries
•If there is an aneurysm, it can bleed into the pericardial sac
•Or if there's a blockage, then can cause an infarct in downstream tissue
•Distribution of Mis
○Circumflex artery obstruction
•Lateral infarction
•20% of cases
○Left anterior descending artery obstruction
•Artery of 'sudden death'
•Anterior infarction
•50% of cases
○Right coronary artery obstruction
•Inferior infarction
•Can involve posterior septum
•30% of cases
•Ischaemia:
○Anaerobic is not as good at aerobic at producing ATP
•It also produces lactic acid as a by-product
○As ATP levels go down, there's less Na+, swelling then necrosis & infarction
○AnginaAngina - pain caused by transient ischaemia
•Angina attack -if swelling goes down before necrosis
•The morphologic changes shown here are indicative of reversible cell
injury
Document Summary
3 layers of the heart: endocardium - inner flattened layer of cells (includes the valves, myocardium - thickest layer, muscle, pericardium - outer layer, 2 membranes that glide over each other. Heart: 4 contractile chambers, right side - pumping blood to lungs for reoxygenation. Left side - pumping blood out to aorta into systemic circulation: movement of blood occurs in response to pressure gradients. High to low pressure environments: direction of movement facilitated by valves, cardiac cycle: Ventricular systole - first phase: ventricular contraction pushes av valves close. Ventricular systole - second phase: ventricular pressure rises and semilunar valves open and blood is ejected. Ventricular diastole - early: as ventricles relax, pressure in ventricles drop, blood flows back and forces semilunar valves closed, blood flows into atria. Ventricular diastole - late: ventricles fill passively. Diastole: when ventricles relax: systole, diastole, co:co: amount of blood ejected from the ventricles every minute. Co = hr x sv: hr =
