Cardiovascular Physiology Lectured by Bien Nillos, MD
Hemodynamics • Arteries – thick walled, extensive
elastic tissue and smooth muscle • Are under high pressure • Blood volume contained in the arteries are called stress volume
• Arterioles – site of highest resistance in the cardiovascular system • Arteriolar resistance is regulated by the autonomic nervous system
• Capillaries – have the largest total cross-sectional and surface area • Are the site of exchange of nutrients , water and gases
• Venules – formed from merged
capillaries • Veins – thin-walled, under low pressure, highest proportion of the blood • Unstressed volume
Velocity of Blood Flow • V = Q/A – – –
Where v = velocity Q = blood flow A = cross-sectional area
– Blood flow velocity is higher in the aorta than in the sum of all of the capillaries
Blood Flow • Q = P/R or • Cardiac output = mean arterial pressure – right arterial pressure Total Peripheral Resistance
Equation of blood flow is analogous to Ohm’s Law Blood flows from high pressure to low pressure
Cardiac Electrophysiology
Cardiac Action Potentials • Resting membrane potential is determined by the conductance to K and approaches the K equilibrium potential • Inward current brings positive charge into the cell and depolarizes the membrane potential • Outward current takes positive charge out of the cell and hyperpolarizes the membrane potential
• Phase 0 – upstroke, increase in Na
conductance. • Phase 1 – initial repolarization, outward current of K, decrease in Na conductance • Phase 2 – plateau, transient increase in Ca conductance, increase in K conductance • Phase 3 – repolarization, Ca conductance decreases and K conductance increases • Phase 4 – resting membrane potential
Excitability • Ability of cardiac cells to initiate action
potentials in response to inward depolarizing current • Absolute refractory Period – begins with the upstroke and ends after the plateau • Effective refractory Period – slightly longer than ARP • Relative refractory Period – period immediately after the ARP
• Chronotropic – changes in the heart rate • Dromotropic – changes in the conduction velocity • Inotropic – contractility of cardiac muscles
• cardiac output increases or
decreases in response to changes in heart rate or stroke volume. When a person stands up, for example, cardiac output falls because of a fall in central venous pressure, which leads to a decrease in stroke volume.
• the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism
• Increased venous return increases the
ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation. This mechanism enables the heart to eject the additional venous return, thereby increasing stroke volume.