N580. Test 3. Quiz 7. Chapters
17-20 Questions and Complete
Solutions Graded A+
How are events of the cardiac cycle reflected in pressure and volume changes within the cardiac
chambers? DIASTOLE - Answer: During diastole the ventricles are relaxed and blood flows in from the
atria through open AV valves. Toward the end of ventricular diastole, the atrial pressure rises, leading to
atrial contraction, which squeezes more blood through the AV valves into the ventricles.
How are events of the cardiac cycle reflected in pressure and volume changes within the cardiac
chambers? SYSTOLE - Answer: Systole includes isovolumic contraction, causing intraventricular pressure
to rise and AV valves to close; the rise in ventricular pressure exceeds aortic pressure and the valves are
forced open, leading to ventricular ejection. Ejection of blood into the aorta causes a rise in aortic
pressure and a fall in ventricular pressure and volume with closing of the semilunar valve and isovolumic
relaxation.
What factors affect the blood supply to myocardial tissue? - Answer: Coronary blood flow is centrally
regulated by the AUTONOMIC nervous system and locally by autoregulation. The amount of coronary
flow depends on driving pressure and coronary resistance, which is dependent on the vessel diameter.
How does sarcomere cross-bridge formation lead to muscle cell contraction? - Answer: Contraction of
cardiac muscle is accomplished by shortening of individual sarcomeres. This is due to increased overlap
of actin and myosin filaments. Myosin heads bind to specific sites on actin and pull the thin filaments
toward the center of the sarcomere, resulting in contraction.
*What is the process of excitation-contraction coupling in heart muscle cells?* - Answer: The spread of
an action potential over cardiac muscle cell surfaces results in myocardial contraction. The resting
membrane potential is determined by the ratio of intracellular to extracellular potassium concentration.
The five phases of the cardiac action potential are due to changes in ion conductance through the
plasma membrane. The main changes in ion conductance result from opening of the fast sodium
channels (phase 0), slow calcium channels (plateau), and potassium channels (repolarization) in plasma
membranes.
"Heart has the NaCK" ... Na+ Ca2+ K+ ... Sodium (Na+) then Calcium (Ca2+) then Potassium (K+)
, What causes myocardial contraction? - Answer: The spread of an action potential over cardiac muscle
cell surfaces
What determines the resting membrane potential in the heart? - Answer: the ratio of intracellular to
extracellular potassium concentration.
* How are action potentials generated and conducted in myocardial and pacemaker cells? * - Answer:
Spontaneous action potentials are generated in automatic cells due to progressive leaking of sodium
and calcium ions into the cell via channels that automatically open during repolarization. The rate of
cation leak determines the rate of pacemaker discharge.
PARASYMPATHETIC influence increases potassium efflux (K+ OUTFLOW) and slows the rate (OF
POTASSIUM OUTFLOW).
SYMPATHETIC influence increases influx of sodium (Na+ IN) and calcium ions (Ca2+ IN) and increases the
rate.
What determines the rate of pacemaker discharge? - Answer: rate of cation leak
*What slows the rate of pacemaker discharge?* - Answer: Parasympathetic influence increases
potassium efflux (i.e. INCREASES K+ MOVEMENT OUT OF THE CELL) and consequently slows the heart
rate.
*What speeds up the rate of pacemaker discharge?* - Answer: SYMPATHETIC influence increases influx
of sodium and calcium ions (RATE OF Na+ and Ca2+ COMING IN) and increases the rate.
How does an electrocardiogram relate to impulse conduction through the heart? - Answer: The
electrocardiogram represents an algebraic sum of all depolarizing and repolarizing currents occurring in
the heart.
How do heart rate, stroke volume, preload, afterload, and contractility affect cardiac output and cardiac
workload? - Answer: An increase in heart rate, stroke volume, preload, or contractility will INCREASE
cardiac output.
Increased afterload will decrease stroke volume, leading to DECREASED cardiac output.
17-20 Questions and Complete
Solutions Graded A+
How are events of the cardiac cycle reflected in pressure and volume changes within the cardiac
chambers? DIASTOLE - Answer: During diastole the ventricles are relaxed and blood flows in from the
atria through open AV valves. Toward the end of ventricular diastole, the atrial pressure rises, leading to
atrial contraction, which squeezes more blood through the AV valves into the ventricles.
How are events of the cardiac cycle reflected in pressure and volume changes within the cardiac
chambers? SYSTOLE - Answer: Systole includes isovolumic contraction, causing intraventricular pressure
to rise and AV valves to close; the rise in ventricular pressure exceeds aortic pressure and the valves are
forced open, leading to ventricular ejection. Ejection of blood into the aorta causes a rise in aortic
pressure and a fall in ventricular pressure and volume with closing of the semilunar valve and isovolumic
relaxation.
What factors affect the blood supply to myocardial tissue? - Answer: Coronary blood flow is centrally
regulated by the AUTONOMIC nervous system and locally by autoregulation. The amount of coronary
flow depends on driving pressure and coronary resistance, which is dependent on the vessel diameter.
How does sarcomere cross-bridge formation lead to muscle cell contraction? - Answer: Contraction of
cardiac muscle is accomplished by shortening of individual sarcomeres. This is due to increased overlap
of actin and myosin filaments. Myosin heads bind to specific sites on actin and pull the thin filaments
toward the center of the sarcomere, resulting in contraction.
*What is the process of excitation-contraction coupling in heart muscle cells?* - Answer: The spread of
an action potential over cardiac muscle cell surfaces results in myocardial contraction. The resting
membrane potential is determined by the ratio of intracellular to extracellular potassium concentration.
The five phases of the cardiac action potential are due to changes in ion conductance through the
plasma membrane. The main changes in ion conductance result from opening of the fast sodium
channels (phase 0), slow calcium channels (plateau), and potassium channels (repolarization) in plasma
membranes.
"Heart has the NaCK" ... Na+ Ca2+ K+ ... Sodium (Na+) then Calcium (Ca2+) then Potassium (K+)
, What causes myocardial contraction? - Answer: The spread of an action potential over cardiac muscle
cell surfaces
What determines the resting membrane potential in the heart? - Answer: the ratio of intracellular to
extracellular potassium concentration.
* How are action potentials generated and conducted in myocardial and pacemaker cells? * - Answer:
Spontaneous action potentials are generated in automatic cells due to progressive leaking of sodium
and calcium ions into the cell via channels that automatically open during repolarization. The rate of
cation leak determines the rate of pacemaker discharge.
PARASYMPATHETIC influence increases potassium efflux (K+ OUTFLOW) and slows the rate (OF
POTASSIUM OUTFLOW).
SYMPATHETIC influence increases influx of sodium (Na+ IN) and calcium ions (Ca2+ IN) and increases the
rate.
What determines the rate of pacemaker discharge? - Answer: rate of cation leak
*What slows the rate of pacemaker discharge?* - Answer: Parasympathetic influence increases
potassium efflux (i.e. INCREASES K+ MOVEMENT OUT OF THE CELL) and consequently slows the heart
rate.
*What speeds up the rate of pacemaker discharge?* - Answer: SYMPATHETIC influence increases influx
of sodium and calcium ions (RATE OF Na+ and Ca2+ COMING IN) and increases the rate.
How does an electrocardiogram relate to impulse conduction through the heart? - Answer: The
electrocardiogram represents an algebraic sum of all depolarizing and repolarizing currents occurring in
the heart.
How do heart rate, stroke volume, preload, afterload, and contractility affect cardiac output and cardiac
workload? - Answer: An increase in heart rate, stroke volume, preload, or contractility will INCREASE
cardiac output.
Increased afterload will decrease stroke volume, leading to DECREASED cardiac output.
