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Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Abnormal heart sounds
Normal heart sounds
Changes in pressure-volume loops
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Law of Laplace
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Cardiac conduction velocity
Electrical conduction in the heart
ECG normal sinus rhythm
ECG QRS transition
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Control of blood flow circulation
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Compliance of blood vessels
Laminar flow and Reynolds number
Pressures in the cardiovascular system
Resistance to blood flow
Action potentials in myocytes
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Excitability and refractory periods
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preload/afterload effects p. 290
auscultation and p. 295
cardiac output p. 289
hydralazine p. 323
in shock p. 317
afterload effects p. 290
Cardiac afterload is one of the main factors that influence how much blood the heart pumps out with each heartbeat, or stroke.
Now, remember that the heart has two upper chambers: the left atrium, which receives oxygenated blood from the lungs via the pulmonary veins; and the right atrium, which receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava.
From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries.
Alright, now, each heartbeat consists of two phases: systole, which is when the heart contracts and pumps the blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood.
And as the left ventricle fills with blood during diastole, the pressure within it rises.
Then the left ventricle contracts, increasing the pressure within the left ventricle even more and forcing blood through the aortic valve into the aorta and whole arterial system.
So, cardiac afterload can be defined as the ventricular wall stress during systole or ejection.
And it can be calculated using the law of Laplace, which states that wall stress = pressure (P) x radius (R) / 2 x wall thickness (W).
Afterload is the amount of work the heart has to do to pump blood to the rest of the body. It's determined by the resistance to flow in the arteries. Blood vessels can become narrower (vasoconstriction) or wider (vasodilation), and this affects afterload.
The heart muscle contracts and relaxes to pump blood. During systole, contraction occurs, which ejects blood from the ventricles into the aorta and other arteries. Then, during diastole, relaxation occurs and blood flows back into the ventricles from the atria.
Afterload directly affects how much force is needed to eject blood from the ventricles during systole. If afterload is high, the ventricles have to work harder to pump blood out, and this can lead to heart failure. There are many factors that can influence the afterload, such as valvular heart diseases, hypertension, and narrowing of arteries by conditions such as atherosclerosis.
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