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Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Electrical conduction in the heart
Cardiac conduction velocity
ECG normal sinus rhythm
ECG QRS transition
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
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preload/afterload effects p. 292
preload/afterload effects p. 292
Filip Vasiljević, MD
Sam Gillespie, BSc
Pauline Rowsome, BSc (Hons)
Cardiac preload 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.
The pressure at the end of diastole is called the left ventricular end-diastolic pressure, which is a key determinant of cardiac preload.
So, cardiac preload can be defined as the ventricular wall stress at the end of diastole.
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).
Another way to say this is that cardiac preload is directly proportional to the end-diastolic pressure and radius of the left ventricle, and indirectly proportional to two times the ventricular wall thickness.
Cardiac preload is the extent to which the left ventricular wall stretches at the end of diastole, or before systole starts. The amount of left ventricular wall stress is directly proportional to the ventricular end-diastolic pressure and the radius of the left ventricle, and indirectly proportional to two times the thickness of the left ventricular wall. Factors that increase preload include an increase in venous return (due to increased venous pressure or increased heart rate), an increase in arterial elastance, or an increase in myocardial contractility. Factors that affect preload include venous return, atrial contraction, heart rate, resistance from valves, and ventricular compliance.
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