Chapter 17 focuses on the cardiovascular system.
The professor will not cover every slide in the PowerPoint but specifies which slides are important.
Material covered verbally and on PowerPoint is testable.
Taking notes alongside the PowerPoint slides is advisable.
Each unit starts with a review of normal anatomy and physiology before discussing pathology.
The professor emphasizes that all necessary information is self-contained within the course, even if students are simultaneously taking Anatomy and Physiology courses.
The primary function of the heart is to efficiently pump blood through the vessels.
Blood flow through the heart is explained to understand the anatomical picture.
Deoxygenated blood from the head, neck, shoulders, and arms returns to the right atrium via the superior vena cava.
Blood from the rest of the body returns to the right atrium via the inferior vena cava.
Deoxygenated blood from the heart itself returns via the coronary sinus and great cardiac vein into the right atrium.
Blood then flows from the right atrium to the right ventricle.
The heart has two atria and two ventricles separated by valves called atrioventricular (AV) valves.
AV valves are anchored by chordae tendineae to papillary muscles in the ventricle walls.
Chordae tendineae prevent AV valves from inverting into the atria during ventricular contraction.
Only AV valves have chordae tendineae; semilunar valves do not need them.
The AV valve on the right side is called the right atrioventricular valve or tricuspid valve.
The AV valve on the left side is called the left atrioventricular valve, mitral valve, or bicuspid valve (due to having two cusps).
During diastole (rest), the atria squeeze blood into the ventricles.
Atrioventricular valves are open, and semilunar valves are closed during this phase.
Preload refers to the volume of blood in the ventricles at the end of diastole.
Cardiovascular exercise can increase preload capacity and stroke volume.
Contractility refers to the force of ventricular contraction.
The amount of contractile proteins in muscle cells is a key factor; this amount can be affected by myocardial infarction (heart attack) or ischemia (reduced oxygen supply).
Myocardial infarction involves the death of heart cells, which contain contractile proteins.
Ischemia can reduce the recruitment of contractile proteins due to insufficient oxygen supply.
Calcium availability is important for myosin to bind to actin.
Afterload is the resistance the ventricles must overcome to eject blood.
Aortic stenosis is an example of increased afterload, where the aortic valve doesn't open enough, causing the left ventricle to work harder.
Elevated blood pressure is another cause of increased afterload.
Cardiac workload depends on preload, contractility, and afterload.
Atrial natriuretic peptide (ANP) is released when the atria are stretched due to excess fluid.
ANP inhibits aldosterone, promoting sodium and water excretion, which lowers blood pressure.
B-type natriuretic peptide (BNP) is released from the ventricles during heart failure or fluid overload.
BNP functions similarly to ANP.
Slides 62 onward cover diagnostic devices.
These devices are only relevant as they are used and explained by the professor.