2025 Physiology Exam 2

Question 1

Pathway of Heartbeat

Answer 1

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.

Question 2

Sinus Node

Answer 2

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.

Question 3

Internodal Fibers

Answer 3

Transmits cardiac impulse throughout atria

Anterior, middle, and posterior internodal pathways

Anterior interatrial band carries impulses to left atrium.

Question 4

Flow of Electrical Impulse

Answer 4

SA Node to Internodal Pathways to AV Node (slows down) to AV Bundles to Purkinje System

Question 5

Parasympathetic Nerves Effects on Heart Rate

Answer 5

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.

Question 6

Sympathetic Nerves Effects on Heart Rate

Answer 6

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.

Question 7

The Heart Anatomy

Answer 7

Question 8

Action Potential of Cardiac Muscle

Answer 8

Know this!!!

Question 9

Refractory Period

Answer 9

Absolute Refractory - can not excite no matter what

Relative refractory - can excite if the stimulus is more than the original

Question 10

Results of Action Potential

Answer 10

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)

Question 11

Actin-Myosin Cycle Post Ca++ Release

Answer 11

???

Question 12

Cardiac Cycle

Answer 12

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: trial wave
QRS: Ventricular wave (hides the atria repolarization)
T: Ventricular repolarization

KNOW THIS GRAPH… tells all need to know about the Cardiac Cycle

Question 13

Ventricular Pressure and Volume Curves

Answer 13

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

Question 14

Ejection Fraction

Answer 14

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

Question 15

Way to Increase Blood Pumped by Heart in a Minute

Answer 15

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

Question 16

Afterload

Answer 16

Amount of blood/pressure to be pumped against

Ex. Left Ventricle = pressure in the Aorta

Question 17

Preload

Answer 17

Amount of blood the heart receives

Question 18

Aortic Pressure Curve

Answer 18

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.

Question 19

Valvular Function

Answer 19

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).

Question 20

Frank-Starling Law of the Heart

Answer 20

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.

Question 21

Pressure-Volume Diagram

Answer 21

1st Heart Sound = Mitral valve closes

2nd Heart Sound = Aortic valve closes

… Happen during systole

Question 22

Pressure-Volume Diagram: Preload

Answer 22

Question 23

Pressure-Volume Diagram: Afterload

Answer 23

Question 24

Autonomic Effects on Heart

Answer 24

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

Question 25

Venous Return and Cardiac Output Must be Equal

Answer 25

Venous return is the quantity of blood flowing from the veins into the right atrium each minute.
… it doesn’t seem to be equal because of how some blood goes to lungs

Cardiac output is the quantity of blood pumped into the aorta each minute by the heart. This is also the quantity of blood that flows through the circulation. Cardiac output is the sum of the blood flows to all the tissues of the body.

Question 26

Control of Cardiac Output by Venous Return

Answer 26

More the heart receives, the more it will pump out

Cardiac output is controlled by venous return. Various factors of the peripheral circulation that affect flow of blood into the heart from the veins are the primary controllers of cardiac output.

Factors:
Muscle Contraction
Gravity
Size of the lumen of the vessels

Question 27

Venous Return Curves: Factors Affecting Venous Return

Answer 27

Three principal factors that affect venous return to the heart from the systemic circulation:
Right Atrial Pressure, which exerts a backward force on the veins to impede flow of blood from the veins into the right atrium.

Degree of filling of the systemic circulation (measured by the mean systemic filling pressure), which forces the systemic blood toward the heart (this is the pressure measured everywhere in the systemic circulation when all flow of blood is stopped).

Resistance to blood flow between the peripheral vessels and the right atrium (resistance to venous return)

Question 28

Resistance to Venous Return

Answer 28

Two thirds of the so-called resistance to venous return is determined by venous resistance, and about one third is determined by the arteriolar and small artery resistance.

A decrease in this resistance to one-half normal allows twice as much flow of blood and, therefore, rotates the curve upward to twice as great a slope.

Conversely, an increase in resistance to twice normal rotates the curve downward to one-half as great a slope.

Venous Resistance is the #1 effector
Q= 1/R

Question 29

Normal EKG

Answer 29

The P wave immediately precedes atrial contraction.

The QRS complex immediately precedes ventricular contraction.

The ventricles remain contracted until a few milliseconds after the end of the T repolarization wave.

The atria remain contracted until repolarized, but an atrial repolarization wave cannot be seen on the EKG because it is obscured by the QRS wave.

The P-Q or P-R interval on the electrocardiogram has a normal value of 0.16 seconds (0.12–0.20).

It is the duration of time between the beginning of the P wave and the beginning of the QRS wave.
This represents the time between the beginning of atrial contraction and the beginning of ventricular contraction.

The Q-T interval has a normal value of 0.36 seconds (0.36–0.40, QTc ≤ 0.46) and is the duration of time from the beginning of the Q wave to the end of the T wave
This approximates the time of ventricular contraction.

The heart rate can be determined with the reciprocal of the time interval between each heartbeat.

R-R interval = 0.83 sec
Heart rate = (60 sec)/(0.83 sec) = 72 beats/minute

Question 30

Flow of Electrical Currents in the Chest Around the Heart

Answer 30

Ventricular depolarization starts at the ventricular septum and the endocardial surfaces of the heart.

The average current flows positively from the base of the heart to the apex.

At the very end of depolarization the current reverses from 1/100 second and flows toward the outer walls of the ventricles near the base (S wave).

Question 31

Vectorial Analysis of EKG

Answer 31

The current in the heart flows from the area of depolarization to the polarized areas (from − to +).

The electrical potential generated can be represented by a vector, with the arrowhead pointing in the positive direction.

The length of the vector is proportional to the voltage of the potential.

The generated potential at any instance can be represented by an instantaneous mean vector.

The normal mean QRS vector is about 59 degrees.

Question 32

P Wave

Answer 32

Begins at sinus node and spreads toward A-V node.

This should give a + vector in leads I, II, and III.

Question 33

Causes of Electrical Axis Deviation: Right

Answer 33

Hypertrophy of right ventricle (right axis shift) is caused by pulmonary hypertension, pulmonary valve stenosis, and interventricular septal defect. All cause slightly prolonged QRS and high voltage.