2025 Physiology Exam 2 Flashcards
Lectures 6-11: Cardiovascular, Vascular and Lymphatics, Chemical Senses, Cardiovascular Physiology
Pathway of Heartbeat
Begins in the sinoatrial (S-A) node… has natural and quickest leakage to Na+
Internodal pathway to atrioventricular (A-V) node
Impulse delayed in A-V node and bundle (allows atria to contract before ventricles to give 20% more blood into ventricle (which is already flowing down due to gravity))
A-V bundle takes impulse into ventricles.
Left and right bundles of Purkinje fibers take impulses to all parts of ventricles.
Sinus Node
Specialized cardiac muscle connected to atrial muscle
Acts as pacemaker because membrane leaks Na+ and membrane potential is −55 to −60mV. The constant leak of Na+ makes resting potential to gradually rise
At −55 mV, fast Na+ channels are inactivated.
When membrane potential reaches −40 mV, slow Na+ and Ca++ channels open causing action potential.
After 100–150 msec Ca++ channels close and K+ channels open more thus returning membrane potential to −55mV.
Normal rate of discharge in sinus node is 70–80/min.
A-V node—40-60/min.
Purkinje fibers—15-40/min.
Sinus node is pacemaker because of its faster discharge rate.
Internodal Fibers
Transmits cardiac impulse throughout atria
Anterior, middle, and posterior internodal pathways
Anterior interatrial band carries impulses to left atrium.
Flow of Electrical Impulse
SA Node to Internodal Pathways to AV Node (slows down) to AV Bundles to Purkinje System
Parasympathetic Nerves Effects on Heart Rate
Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate S-A node and A-V junctional fibers proximal to A-V node.
Acetylcholine decreases SN discharge and excitability of A-V fibers, slowing the heart rate.
Cause hyperpolarization because of increased K+ permeability in response to acetylcholine (increased negativity inside)
This causes decreased transmission of impulses maybe temporarily stopping heart rate.
Ventricular escape occurs.
Sympathetic Nerves Effects on Heart Rate
Releases norepinephrine at sympathetic ending
Causes increased sinus node discharge
Increases rate of conduction of impulse
Increases force of contraction in atria and ventricles
Norepinephrine increases permeability to Na+ and Ca+, causing a more + resting potential, accelerating self-excitation, and excitability of AV fibers.
The Heart Anatomy
Action Potential of Cardiac Muscle
Know this!!!
Refractory Period
Absolute Refractory - can not excite no matter what
Relative refractory - can excite if the stimulus is more than the original
Results of Action Potential
Ca++ release from T- tubules, which are large, is a very important source of Ca++.
T-tubule Ca++ depends strongly on extracellular Ca++ concentration.
Heart’s T-tubules are bigger than those in skeletal muscle and rich in mucopolysaccharides.
Mucopolysaccharides bind and store Ca++.
Ca++ release from sarcoplasmic reticulum (after stimulation of ryanodine receptors)
Actin-Myosin Cycle Post Ca++ Release
Steps of the actin-myosin cycle
Ca++ release: Nerve impulses trigger the release of Ca++ from the SR.
Ca++ binding: Ca++ binds to troponin C, which shifts tropomyosin.
Cross-bridge formation: Myosin heads bind to actin filaments, forming cross-bridges.
Power stroke: Myosin heads flex, pulling actin filaments into the myosin channel.
ADP release: ADP is released from the myosin head.
ATP binding: ATP attaches to myosin, allowing the cycle to repeat.
Regulation of the cycle
The cycle continues as long as Ca++ ions remain bound to troponin and ATP is available.
Muscle contraction usually stops when signaling from the motor neuron ends.
Muscle fatigue
Muscle contraction can also stop when the muscle runs out of ATP and becomes fatigued.
Cardiac Cycle
Systole: ventricular muscle stimulated by action potential and contracting (electrical conducting system)
Diastole: ventricular muscle reestablishing Na+/K+/Ca++ gradient and is relaxing
EKG
P: atrial wave
QRS: Ventricular wave (hides the atria repolarization)
T: Ventricular repolarization
KNOW THIS GRAPH… tells all need to know about the Cardiac Cycle
Ventricular Pressure and Volume Curves
Diastole
Isovolumic relaxation
A-V valves open
Rapid inflow
Diastasis—slow flow into ventricle
Atrial systole—extra blood in and follows P wave
Accounts for 10–25% of filling
*** Coronary arteries get filled during the diastole due to the back fill of blood
Systole
Isovolumic contraction
A-V valves close (ventricular press > atrial press)
Aortic valve opens
Ejection phase
Aortic valve closes
Ejection Fraction
End diastolic volume = 120 mL
End systolic volume = 50 mL
Ejection volume (stroke volume) = 70 mL
Ejection fraction = 70 mL/120 mL = 58%
(normally 60%)
If heart rate (HR) is 70 beats/minute, what is cardiac output?
Cardiac output = HR * stroke volume = 70/min * 70 mL = 4900 mL/min
Way to Increase Blood Pumped by Heart in a Minute
Chronotropic = beat faster, contract more often
Inotropic = beat harder, contraction harder
However, blood can only pump out the amount of blood it receives = Preload = Venous Return
Afterload
Amount of blood/pressure to be pumped against
Ex. Left Ventricle = pressure in the Aorta
Preload
Amount of blood the heart receives
Aortic Pressure Curve
Aortic pressure starts increasing during systole after the aortic valve opens.
Aortic pressure decreases toward the end of the ejection phase.
After the aortic valve closes an incisura occurs because of sudden cessation of back-flow toward left ventricle.
Aortic pressure decreases slowly during diastole because of the elasticity of the aorta plus blood flow to the periphery.
Valvular Function
To prevent back-flow
The close and open passively, driven by pressure: backward pressure-close; forward pressure-open
Chordae tendineae are attached to AV valves
Papillary muscle, attached to chordae tendineae, contract during systole and help prevent back-flow (keep them tight).
Due to smaller opening, velocity through aortic and pulmonary valves exceeds that through the Avs.
Most work is external work or pressure-volume work.
A small amount of work is required to impart kinetic energy to the heart (1/2 mV2).
What is stroke volume in Figure 9-11?
External work is area of P–V curve.
Work output is affected by “preload” (end-diastolic pressure) and “afterload” (aortic pressure).
Frank-Starling Law of the Heart
More stretch on the heart, more forceful the contractions… to a point because then actin-myosin can’t overlap anymore to help create more forceful a contraction
Within physiological limits the heart pumps all the blood that comes to it without excessive damming in the veins.
Extra stretch on cardiac myocytes makes actin and myosin filaments interdigitate to a more optimal degree for force generation.
Pressure-Volume Diagram
1st Heart Sound = Mitral valve closes
2nd Heart Sound = Aortic valve closes
… Happen during systole
Pressure-Volume Diagram: Preload
Pressure-Volume Diagram: Afterload
Autonomic Effects on Heart
Sympathetic stimulation causes increased heart rate, increased contractility, and vascular tone.
Parasympathetic stimulation decreases heart rate markedly and cardiac contractility slightly.
Vagal fibers go mainly to atria.
Fast heart rate (tachycardia) can decrease cardiac output because there is not enough time for heart to fill during diastole.
ANS = viscera efferent (controls the motor function of viscera)… any internal organ
Viscera = plural organs
Viscus = singular organ