Veterinary Physiology Exam 3 UPDATED
ACTUAL Exam Questions and CORRECT
Answers
Sinoatrial (SA) node - CORRECT ANSWER - Node of right atrial wall near entrance for
superior vena cava that originates action potentials and establishes normal heart rate
Atrioventricular (AV) node - CORRECT ANSWER - Node between atria and ventricles
that serves as emergency pacemaker for ventricles; slow conduction velocity and long refractory
period creates delay between atrial and ventricular contractions, allowing adequate ventricle
refilling and preventing AP from circling back
AV bundle (bundle of His) - CORRECT ANSWER - One area has slow conduction
velocity and long refractory periods that creates delay between atrial and ventricular
contractions, other has rapid AP conduction causing nearly synchronous contraction of all fibers
in both ventricles
Action Potential Propagation through Ectopic Pacemaker Cells - CORRECT ANSWER -
1. AP from SA node enters normal myocardium
2. Barrier between normal and abnormal myocardium prevents bidirectional propagation of AP
3. AP reaches abnormal myocardium from other side
4. AP propagation slows down in abnormal myocardium, cells originally exposed to AP from SA
node already past refractory period
Progression of Pacemaker Potential - CORRECT ANSWER - 1. Prepotential: slow Na
influx via spontaneous Na channel opening, K and both Ca channels closed
2. Depolarization: both Ca channels open once threshold reached, Na channel still open
3. Repolarization: K channels open once peak membrane potential reached, Na and both Ca
channels close
4. Resting potential re-achieved
, Progression of Cardiac Action Potential - CORRECT ANSWER - - Phase 0: cell reaches
threshold → K and fast Na channels open → rapid depolarization
- Phase 1: Na channels quickly close, K channels stay open → repolarization starts
- Phase 2: some K channels close, slow membrane Ca channels open → Ca enters cell Ca → SR
Ca channels open → membrane stays depolarized for prolonged time period
- Muscle contracts
- Phase 3: K channels reopen, Ca channels reclose → repolarization continues
- Phase 4: all channels closed, resting potential
Effects of Norepinephrine/Epinephrine on Pacemaker Cells - CORRECT ANSWER -
Elevate heartrate, AP strength and AP frequency
Effects of Acetylcholine on Pacemaker Cells - CORRECT ANSWER - Decrease heartrate,
AP strength and AP frequency
Effects of Norepinephrine/Epinephrine on Cardiac Muscle Cells - CORRECT ANSWER -
- Shorter AP, longer phase 2: more slow Ca channels open → longer depolarization state → K
channels open sooner → repolarization goes faster
- Stronger and quicker contractions: more slow Ca channels open → more Ca from extracellular
environment and SR enters cytosol → Ca pumps speed up → Ca taken back into SR or sent back
outside cell faster
Effects of Acetylcholine on Cardiac Muscle Cells - CORRECT ANSWER - - Indirectly
inhibits norepinephrine release from sympathetic neuron terminals
- Weakens effect of sympathetic activation on ventricular cell
- Directly bind to atrial and some ventricular cells
Sick sinus syndrome - CORRECT ANSWER - - Extreme: SA node completely fails to
form APs → AV node keeps ventricles beating at low rate
- Less extreme: sluggish depolarization of SA node → abnormally low HR at rest and
insufficient HR increase during exercise
ACTUAL Exam Questions and CORRECT
Answers
Sinoatrial (SA) node - CORRECT ANSWER - Node of right atrial wall near entrance for
superior vena cava that originates action potentials and establishes normal heart rate
Atrioventricular (AV) node - CORRECT ANSWER - Node between atria and ventricles
that serves as emergency pacemaker for ventricles; slow conduction velocity and long refractory
period creates delay between atrial and ventricular contractions, allowing adequate ventricle
refilling and preventing AP from circling back
AV bundle (bundle of His) - CORRECT ANSWER - One area has slow conduction
velocity and long refractory periods that creates delay between atrial and ventricular
contractions, other has rapid AP conduction causing nearly synchronous contraction of all fibers
in both ventricles
Action Potential Propagation through Ectopic Pacemaker Cells - CORRECT ANSWER -
1. AP from SA node enters normal myocardium
2. Barrier between normal and abnormal myocardium prevents bidirectional propagation of AP
3. AP reaches abnormal myocardium from other side
4. AP propagation slows down in abnormal myocardium, cells originally exposed to AP from SA
node already past refractory period
Progression of Pacemaker Potential - CORRECT ANSWER - 1. Prepotential: slow Na
influx via spontaneous Na channel opening, K and both Ca channels closed
2. Depolarization: both Ca channels open once threshold reached, Na channel still open
3. Repolarization: K channels open once peak membrane potential reached, Na and both Ca
channels close
4. Resting potential re-achieved
, Progression of Cardiac Action Potential - CORRECT ANSWER - - Phase 0: cell reaches
threshold → K and fast Na channels open → rapid depolarization
- Phase 1: Na channels quickly close, K channels stay open → repolarization starts
- Phase 2: some K channels close, slow membrane Ca channels open → Ca enters cell Ca → SR
Ca channels open → membrane stays depolarized for prolonged time period
- Muscle contracts
- Phase 3: K channels reopen, Ca channels reclose → repolarization continues
- Phase 4: all channels closed, resting potential
Effects of Norepinephrine/Epinephrine on Pacemaker Cells - CORRECT ANSWER -
Elevate heartrate, AP strength and AP frequency
Effects of Acetylcholine on Pacemaker Cells - CORRECT ANSWER - Decrease heartrate,
AP strength and AP frequency
Effects of Norepinephrine/Epinephrine on Cardiac Muscle Cells - CORRECT ANSWER -
- Shorter AP, longer phase 2: more slow Ca channels open → longer depolarization state → K
channels open sooner → repolarization goes faster
- Stronger and quicker contractions: more slow Ca channels open → more Ca from extracellular
environment and SR enters cytosol → Ca pumps speed up → Ca taken back into SR or sent back
outside cell faster
Effects of Acetylcholine on Cardiac Muscle Cells - CORRECT ANSWER - - Indirectly
inhibits norepinephrine release from sympathetic neuron terminals
- Weakens effect of sympathetic activation on ventricular cell
- Directly bind to atrial and some ventricular cells
Sick sinus syndrome - CORRECT ANSWER - - Extreme: SA node completely fails to
form APs → AV node keeps ventricles beating at low rate
- Less extreme: sluggish depolarization of SA node → abnormally low HR at rest and
insufficient HR increase during exercise
