N5315 Advanced Pathophysiology
Cardiovascular
Core Concepts and Objectives with Advanced Organizers
Examine the anatomy and physiology of the cardiovascular system.
Cardiovascular Anatomy and Physiology
1. Explain the cardiac structure and blood flow through the heart chambers/valves.
-Heart has 4 chanbers: right atrium, left atrium, right ventricle, left ventricle.
-these chambers form 2 pumps in series: right heart is low-pressure system pumping
blood through the lungs; left heart high-pressure system pumping blood through the
rest of the body.
-atria are smaller than ventricles and have thinner walls 1-2 mm thick.
-ventricle- thicker myocardial layer and make up bulk of the heart. right: 4-5 mm
thick; left: 12-15 mm.
-thickness of each chamber depends of amt of pressure or resistance it must
overcome to eject blood.
-right ventricle: crescent shape, or triangle; efficient large volumes of blood through
semi lunar valve into low-pressure pulm system.
-left ventricle: larger and bullet shaped; helps to eject blood through large aortic
semilunar valve into high-pressure systemic circulation.
Chambers and valves of the heart:figure 31-4 on pg 1087
-A. During atrial contraction cardiac muscle in the atrial wall contracts, forcing blood
through the atrioventricular (2 AV) valves and into the ventricles. Semilunar (SL)
valves closed and AV valves open.
-B. During ventricular contraction that follows, AV valves close and blood is forced out
of ventricle through the SL valves and into the arteries.
2. Describe which coronary arteries provide blood to which part of the heart. ; pg 1088
Great vessels:
-right heart receives venous deoxygenated blood from systemic circulation through
the superior vena cava and inferior vena cava, which enter the right atrium. Blood
leaves the right ventricle and enters the pulm circulation through the pulm artery.
The pulm artery divides into right and left pulmonary arteries to transport
unoxygenated blood from the right heart to the right and left lungs. The pulm arteries
branch further into pulm capillary bed, where oxygen enters the blood and carbon
dioxide leaves it as each gas moves from its higher to lower concentration gradient. 4
pulm veins, 2 from right lung and 2 from left lung, carry oxygenated blood from lungs
to the left side of the heart. Oxygenated blood moves through the left atrium and
ventricle and out into the aorta, delivering it to systemic vessels that supply the
body.
Coronary Arteries; pg 1090-1091:
-Major coronary arteries: Right coronary artery (RCA) and left coronary artery (LCA)
-RCA has greater flow than LCA
-coronary arteries are smaller in women than men due to diff in height and weight
-LAC divides into left anterior descending (LAD) artery and Circumflex artery. LAD
delivers blood to portions of the left and right ventricles and much of interventricular
septum. LAD travels in groove btw L/R ventricle doen anterior septum of intraventricular
septum toward apex of heart.; Circumflex artery travels in groove, coronary salcus,
separating left atrium and left ventricle to left border of heart. Supplies blood to the left
,atrium and lateral wall of the left ventricle. Circumflex artery branches to posterior surface
of the left atrium and left ventricle.
-RCA originates from ostium behind the right aortic cusp travelling behind pulm artery,
and extending around the right heart to the heart’s posterior surface, where it branches to
the right atrium and ventricle.
-3 major branches of RCA: conus(supplying blood to upper right ventricle), right marginal
branch (traverses right ventricle to the apex), and posterior descending branch, which lies in
the posterior interventricular sulcus and supplies smaller branches to both ventricles.
3. Analyze the process of cardiac action potentials. ; lecture specifies to know phase 0-4
in the cardiac action potential lecture
4. Ventricular Action Potential generated from Bundle of His or Purkinji Fibers, 5
phases.
a. Resting membrane potential is ~-85mV.
b. Phase 0: Rapid depolarization (less negative) of the cell. Na+ influx as the
result of voltage gated Na+ channels opening
c. Phase 1: Initial repolarization (more negative) of the cells. Voltage gates Na+
channels are closed, voltage gages K+ channels being to open and K+ leaves
the cell.
d. Phase 2: Plateau change. Ca+ channels open, influx of Ca+ into the cells. This
balances out K+ efflux thus causing a temporary plateau in repolarization.
Influx of Ca+ triggers release of more calcium from the sarcoplasmic
reticulum and thus massive myocardial contraction.
e. Phase 3: Rapid repolarization with massive K+ efflux. Voltage gated K+
channels open, voltage gated Ca+ close, causes rapid repolarization.
f. Phase 4: Resting membrane potential of -85mV. High potassium permeability
from potassium channels.
5. SA & AV Node Generation
a. 3 Phases
b. Phase 0: Depolarization from the opening of voltage gated Ca+ channels.
Voltage gated Na+ are inactivated. *Slow conduction of the impulse which is
used by the AV node to prolong transmission from the atria to the ventricles*
c. Phase 3: Repolarization, from the closure of the voltage gated Ca+ channels,
opening of voltage gated K+ channels.
d. Phase 4: Slow depolarization from the slow, spontaneous efflux of Na+. This
gives the SA & AV nodes the property of automaticity. Do not need stimulus,
automatically generate action potential.
e. Acetylcholine and Adenosine cause a decrease in the rate of depolarization
and decrease heart rate.
f. Catecholamines increase the rate of depolarization and increase heart rate.
6. Discuss how potassium and calcium imbalances affect myocardial action potentials,
contraction, and the clinical manifestations which result.
Hypokalemia: Extracellular K+ is depleted, so K+ inside the cell can diffuse more
easily. The cell is HYPERpolarized (more negative) so the cell will need a larger than
normal stimulus to reach threshold potential.
a. Clinical manifestations: weakness, smooth muscle atony, paresthesias, U
wave sometimes present on EKG, and cardiac dysrhythmias
Hyperkalemia: When extracellular K+ increases, with no change to intracellular K+,
the resting membrane potential becomes more positive. The cell is HYPOpolarized
(more positive) and is more excitable.
, b. Clinical manifestations: Peak T waves of EKG, cardiac standstill, paralysis,
paresthesias
Hypocalcemia: Increase the cell permeability to sodium… causes threshold potential
to be more negative and closer to the resting potential. Can cause an action potential
more often. MORE excitability
c. Clinical manifestations: Tetany, hyperreflexia, circumoral paresthesia,
seizures, and dysrhythmias
Hypercalcemia: Decreased cell permeability to sodium...threshold potential
becomes more positive, so more stimulus is needed to conduct action potential. LESS
excitable
d. weakness, hyporeflexia, encephalopathy, shortened QT segment and
depressed widened T-waves on EKG
7. Discuss the effect of a magnesium imbalance on the cardiovascular system.
Magnesium is required for the binding of ATP to the myosin sites. The splitting of ATP
occurs on the myosin molecure before it attaches to actin. ATP breakdown to ADP and
inorganic phosphate is required in order to gain the energy needed for movement of
the cross bridge formed for contraction of cardiac cells.
In addition to being necessary for binding of the ATP to the myosin sites for the
functionality of the cross-bridges, magnesium, potassium, calcium is necessary for
the myocardial cells along with oxygen to maintain normal contractility. O2
deprivation also is accompanied by electrolyte disturbances, specifically, loss of
potassium, calcium, and magnesium from the cells. Myocardial cells deprived of
necessary oxygen and nutrients lose contractility, thereby diminishing the heart’s
pumping ability. P. 1158
8. Explain the difference between cardiac hemodynamic measures: Cardiac output,
stroke volume, ejection fraction, preload and afterload.
Cardiac Output: Volume of blood flowing through systemic or pulmonary circuit (L/min)
(CO= HR (bpm) x SV)
Stroke Volume: Volume of blood pumped from the left ventricle; normal ~70ml
(SV = End Diastolic Volume - End Systolic1 Volume)
Ejection Fraction: Amount of blood ejected with each heartbeat
(EF=SV/End Diastolic Volume)
Preload: Pressure generated at the end of diastole;
Clinician measures indexes of Left Ventricular End-Diastolic Pressure (p.1103)
Afterload: Left Ventricular End-Diastolic Pressure;
Clinician measures aortic systolic pressure (p.1103)
9. Analyze factors which affect cardiac contractility.
Electrolyte imbalances, Hypoxia, blood clots
Cardiovascular
Core Concepts and Objectives with Advanced Organizers
Examine the anatomy and physiology of the cardiovascular system.
Cardiovascular Anatomy and Physiology
1. Explain the cardiac structure and blood flow through the heart chambers/valves.
-Heart has 4 chanbers: right atrium, left atrium, right ventricle, left ventricle.
-these chambers form 2 pumps in series: right heart is low-pressure system pumping
blood through the lungs; left heart high-pressure system pumping blood through the
rest of the body.
-atria are smaller than ventricles and have thinner walls 1-2 mm thick.
-ventricle- thicker myocardial layer and make up bulk of the heart. right: 4-5 mm
thick; left: 12-15 mm.
-thickness of each chamber depends of amt of pressure or resistance it must
overcome to eject blood.
-right ventricle: crescent shape, or triangle; efficient large volumes of blood through
semi lunar valve into low-pressure pulm system.
-left ventricle: larger and bullet shaped; helps to eject blood through large aortic
semilunar valve into high-pressure systemic circulation.
Chambers and valves of the heart:figure 31-4 on pg 1087
-A. During atrial contraction cardiac muscle in the atrial wall contracts, forcing blood
through the atrioventricular (2 AV) valves and into the ventricles. Semilunar (SL)
valves closed and AV valves open.
-B. During ventricular contraction that follows, AV valves close and blood is forced out
of ventricle through the SL valves and into the arteries.
2. Describe which coronary arteries provide blood to which part of the heart. ; pg 1088
Great vessels:
-right heart receives venous deoxygenated blood from systemic circulation through
the superior vena cava and inferior vena cava, which enter the right atrium. Blood
leaves the right ventricle and enters the pulm circulation through the pulm artery.
The pulm artery divides into right and left pulmonary arteries to transport
unoxygenated blood from the right heart to the right and left lungs. The pulm arteries
branch further into pulm capillary bed, where oxygen enters the blood and carbon
dioxide leaves it as each gas moves from its higher to lower concentration gradient. 4
pulm veins, 2 from right lung and 2 from left lung, carry oxygenated blood from lungs
to the left side of the heart. Oxygenated blood moves through the left atrium and
ventricle and out into the aorta, delivering it to systemic vessels that supply the
body.
Coronary Arteries; pg 1090-1091:
-Major coronary arteries: Right coronary artery (RCA) and left coronary artery (LCA)
-RCA has greater flow than LCA
-coronary arteries are smaller in women than men due to diff in height and weight
-LAC divides into left anterior descending (LAD) artery and Circumflex artery. LAD
delivers blood to portions of the left and right ventricles and much of interventricular
septum. LAD travels in groove btw L/R ventricle doen anterior septum of intraventricular
septum toward apex of heart.; Circumflex artery travels in groove, coronary salcus,
separating left atrium and left ventricle to left border of heart. Supplies blood to the left
,atrium and lateral wall of the left ventricle. Circumflex artery branches to posterior surface
of the left atrium and left ventricle.
-RCA originates from ostium behind the right aortic cusp travelling behind pulm artery,
and extending around the right heart to the heart’s posterior surface, where it branches to
the right atrium and ventricle.
-3 major branches of RCA: conus(supplying blood to upper right ventricle), right marginal
branch (traverses right ventricle to the apex), and posterior descending branch, which lies in
the posterior interventricular sulcus and supplies smaller branches to both ventricles.
3. Analyze the process of cardiac action potentials. ; lecture specifies to know phase 0-4
in the cardiac action potential lecture
4. Ventricular Action Potential generated from Bundle of His or Purkinji Fibers, 5
phases.
a. Resting membrane potential is ~-85mV.
b. Phase 0: Rapid depolarization (less negative) of the cell. Na+ influx as the
result of voltage gated Na+ channels opening
c. Phase 1: Initial repolarization (more negative) of the cells. Voltage gates Na+
channels are closed, voltage gages K+ channels being to open and K+ leaves
the cell.
d. Phase 2: Plateau change. Ca+ channels open, influx of Ca+ into the cells. This
balances out K+ efflux thus causing a temporary plateau in repolarization.
Influx of Ca+ triggers release of more calcium from the sarcoplasmic
reticulum and thus massive myocardial contraction.
e. Phase 3: Rapid repolarization with massive K+ efflux. Voltage gated K+
channels open, voltage gated Ca+ close, causes rapid repolarization.
f. Phase 4: Resting membrane potential of -85mV. High potassium permeability
from potassium channels.
5. SA & AV Node Generation
a. 3 Phases
b. Phase 0: Depolarization from the opening of voltage gated Ca+ channels.
Voltage gated Na+ are inactivated. *Slow conduction of the impulse which is
used by the AV node to prolong transmission from the atria to the ventricles*
c. Phase 3: Repolarization, from the closure of the voltage gated Ca+ channels,
opening of voltage gated K+ channels.
d. Phase 4: Slow depolarization from the slow, spontaneous efflux of Na+. This
gives the SA & AV nodes the property of automaticity. Do not need stimulus,
automatically generate action potential.
e. Acetylcholine and Adenosine cause a decrease in the rate of depolarization
and decrease heart rate.
f. Catecholamines increase the rate of depolarization and increase heart rate.
6. Discuss how potassium and calcium imbalances affect myocardial action potentials,
contraction, and the clinical manifestations which result.
Hypokalemia: Extracellular K+ is depleted, so K+ inside the cell can diffuse more
easily. The cell is HYPERpolarized (more negative) so the cell will need a larger than
normal stimulus to reach threshold potential.
a. Clinical manifestations: weakness, smooth muscle atony, paresthesias, U
wave sometimes present on EKG, and cardiac dysrhythmias
Hyperkalemia: When extracellular K+ increases, with no change to intracellular K+,
the resting membrane potential becomes more positive. The cell is HYPOpolarized
(more positive) and is more excitable.
, b. Clinical manifestations: Peak T waves of EKG, cardiac standstill, paralysis,
paresthesias
Hypocalcemia: Increase the cell permeability to sodium… causes threshold potential
to be more negative and closer to the resting potential. Can cause an action potential
more often. MORE excitability
c. Clinical manifestations: Tetany, hyperreflexia, circumoral paresthesia,
seizures, and dysrhythmias
Hypercalcemia: Decreased cell permeability to sodium...threshold potential
becomes more positive, so more stimulus is needed to conduct action potential. LESS
excitable
d. weakness, hyporeflexia, encephalopathy, shortened QT segment and
depressed widened T-waves on EKG
7. Discuss the effect of a magnesium imbalance on the cardiovascular system.
Magnesium is required for the binding of ATP to the myosin sites. The splitting of ATP
occurs on the myosin molecure before it attaches to actin. ATP breakdown to ADP and
inorganic phosphate is required in order to gain the energy needed for movement of
the cross bridge formed for contraction of cardiac cells.
In addition to being necessary for binding of the ATP to the myosin sites for the
functionality of the cross-bridges, magnesium, potassium, calcium is necessary for
the myocardial cells along with oxygen to maintain normal contractility. O2
deprivation also is accompanied by electrolyte disturbances, specifically, loss of
potassium, calcium, and magnesium from the cells. Myocardial cells deprived of
necessary oxygen and nutrients lose contractility, thereby diminishing the heart’s
pumping ability. P. 1158
8. Explain the difference between cardiac hemodynamic measures: Cardiac output,
stroke volume, ejection fraction, preload and afterload.
Cardiac Output: Volume of blood flowing through systemic or pulmonary circuit (L/min)
(CO= HR (bpm) x SV)
Stroke Volume: Volume of blood pumped from the left ventricle; normal ~70ml
(SV = End Diastolic Volume - End Systolic1 Volume)
Ejection Fraction: Amount of blood ejected with each heartbeat
(EF=SV/End Diastolic Volume)
Preload: Pressure generated at the end of diastole;
Clinician measures indexes of Left Ventricular End-Diastolic Pressure (p.1103)
Afterload: Left Ventricular End-Diastolic Pressure;
Clinician measures aortic systolic pressure (p.1103)
9. Analyze factors which affect cardiac contractility.
Electrolyte imbalances, Hypoxia, blood clots
