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.
2. Describe which coronary arteries provide blood to which part of the heart.
3. Analyze the process of cardiac action potentials.
4. Discuss how potassium and calcium imbalances affect myocardial action potentials,
contraction, and the clinical manifestations which result.
5. Discuss the effect of a magnesium imbalance on the cardiovascular system.
6. Explain the difference between cardiac hemodynamic measures: Cardiac output, stroke
volume, ejection fraction, preload and afterload.
Cardiac Output The amount of blood the heart pumps in 1
minute. It’s equal to the heart rate multiplied
by the stroke volume.
Stroke Volume The amount of blood ejected with each
heartbeat
Ejection Fraction The percentage of blood ejected from the left
ventricle with each contraction (beat)
Preload The initial stretching of the cardiac myocytes
(muscle cells) prior to contraction. AKA Left
ventricular end-diastolic pressure (LVEDP)
Afterload Resistance/force the left ventricle must
overcome to circulate blood
7. Analyze factors which affect cardiac contractility.
a. Explain the normal function of myocardial cells.
b. Explain the process of cardiac contraction and relaxation.
c. Evaluate the effects of the catecholamines on the cardiovascular system.
Catecholamine Effect on the CV system
Epinephrine Epinephrine primarily stimulates the beta 1 receptors of the heart
which results in an increase in myocardial contractility and heart rate.
Some simultaneous effects on both the beta 2 and alpha 1 receptors.
The simultaneous stimulation of these two receptors by epinephrine
results in a cancelation of their individual functions and thus the
vascular tone does not change. When epinephrine is administered as a
drug its main purpose is to increase contractility. When it is
, administered in high doses its alpha 1 effects override the beta 2
effects which causes vasoconstriction and increased systemic vascular
resistance while still enhancing myocardial contractility and cardiac
output. Released by adrenal cortex; causes vasoconstriction in most
vascular beds except the coronary, liver and skeletal muscle
circulations. It dilates the coronary, liver and skeletal vessels, thus
causing an increase in myocardial contractility; stimulates Beta 1
receptors of the heart which results in an increase myocardial
contractility and heart rate. It also has some effect on Beta 2 and
Alpha 1 receptors; enhances cardiac output
Norepinephrin Stimulates beta 1and alpha 1 receptors. This increases myocardial
e contractility and causes vasoconstriction. These physiologic changes
result in an increase in cardiac output and blood pressure. This is the
basis of the drug norepinephrine (levophed)
Dopamine Dopamine is administered at low doses it
predominantly stimulates the dopamine 1 receptors
and causes vasodilation. When moderate doses are
administered it stimulates the beta 1 receptors and
improves myocardial contractility and cardiac output.
At high doses dopamine has alpha 1 activity and causes
vasoconstriction. Dobutamine stimulates the beta 1
receptors in the myocardium and improves contractility
and increases heart rate. Precursor to epinephrine and
norepinephrine; stimulates the dopamine 1 receptors
and causes vasodilation; when moderate doses are
given, it stimulates the beta 1 receptors and improves
contractility and cardiac output. High doses has alpha
1 effects causing vasoconstriction.
d. Describe pathologic and physiologic factors which increase or decrease
myocardial contraction.
Factors which Increase Cardiac Factors which Decrease Cardiac
Contraction Contraction
Catecholamines-increase the activity of Beta blockers-block the effect of the
the calcium pump in the sarcoplasmic catecholamines
reticulum; therefore, it increase the
release of calcium from SR
Increases in the intracellular calcium Heart failure with systolic dysfunction
Decrease extracellular sodium-decreases Acidosis
the activity of Na/Ca exchanger
Digitalis-blocks the Na/K pump which Hypoxia/hypercapnia
increases the intracellular Na, decreases
the activity of the Na/Ca exchanger, and
, increases the intracellular Ca
Nondihydropyridine calcium channel
blockers (Diltiazem, Verapamil)
e. Describe how diltiazem, verapamil, digitalis, beta blockers and dobutamine affect
myocardial contraction.
Medication Increases or decreases How does it increase or Clinical Implications
contraction decrease contraction?
Diltiazem & Decreases They inhibit the influx These medication
Verapamil of calcium into the should be avoided in
myocardium. This persons with systolic
decreases the heart failure. Helpful
intracellular calcium for HTN, prinzmetal
concentration which in angina
turn decreases the
myocardial tension and
contractility. They have
negative inotrophic
effects.
Vasodilation= decrease
BP, decrease
SVR=decrease afterload
Digitalis Increases
Beta Blockers Decreases
Dobutamine Increases; increases HR Synthetic
(chronotrophy) and catecholamine, direct
lowers the afterload beta 1 agonist and some
beta 2 and alpha 1
effects
Beta 2 stimulation
causes vasodilation
(lower afterload)
Aging and the Cardiovascular System
1. Describe how the normal anatomy and physiology of the arteries and left ventricle are
altered by the aging process.
2. Explain the prenatal and post-natal development of the cardiovascular system.
3. Differentiate between the effects of aging on the anatomical and physiologic processes of
the cardiovascular system.
Cardiovascular Effects of aging
structure / Process
Cardiac Index: A slight decrease in the cardiac index for women while at rest.
During exercise the CI decreased for both genders because of
decrease in HR and stroke volume
Heart Rate The resting HR decreases but during exercise the increase in HR is
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.
2. Describe which coronary arteries provide blood to which part of the heart.
3. Analyze the process of cardiac action potentials.
4. Discuss how potassium and calcium imbalances affect myocardial action potentials,
contraction, and the clinical manifestations which result.
5. Discuss the effect of a magnesium imbalance on the cardiovascular system.
6. Explain the difference between cardiac hemodynamic measures: Cardiac output, stroke
volume, ejection fraction, preload and afterload.
Cardiac Output The amount of blood the heart pumps in 1
minute. It’s equal to the heart rate multiplied
by the stroke volume.
Stroke Volume The amount of blood ejected with each
heartbeat
Ejection Fraction The percentage of blood ejected from the left
ventricle with each contraction (beat)
Preload The initial stretching of the cardiac myocytes
(muscle cells) prior to contraction. AKA Left
ventricular end-diastolic pressure (LVEDP)
Afterload Resistance/force the left ventricle must
overcome to circulate blood
7. Analyze factors which affect cardiac contractility.
a. Explain the normal function of myocardial cells.
b. Explain the process of cardiac contraction and relaxation.
c. Evaluate the effects of the catecholamines on the cardiovascular system.
Catecholamine Effect on the CV system
Epinephrine Epinephrine primarily stimulates the beta 1 receptors of the heart
which results in an increase in myocardial contractility and heart rate.
Some simultaneous effects on both the beta 2 and alpha 1 receptors.
The simultaneous stimulation of these two receptors by epinephrine
results in a cancelation of their individual functions and thus the
vascular tone does not change. When epinephrine is administered as a
drug its main purpose is to increase contractility. When it is
, administered in high doses its alpha 1 effects override the beta 2
effects which causes vasoconstriction and increased systemic vascular
resistance while still enhancing myocardial contractility and cardiac
output. Released by adrenal cortex; causes vasoconstriction in most
vascular beds except the coronary, liver and skeletal muscle
circulations. It dilates the coronary, liver and skeletal vessels, thus
causing an increase in myocardial contractility; stimulates Beta 1
receptors of the heart which results in an increase myocardial
contractility and heart rate. It also has some effect on Beta 2 and
Alpha 1 receptors; enhances cardiac output
Norepinephrin Stimulates beta 1and alpha 1 receptors. This increases myocardial
e contractility and causes vasoconstriction. These physiologic changes
result in an increase in cardiac output and blood pressure. This is the
basis of the drug norepinephrine (levophed)
Dopamine Dopamine is administered at low doses it
predominantly stimulates the dopamine 1 receptors
and causes vasodilation. When moderate doses are
administered it stimulates the beta 1 receptors and
improves myocardial contractility and cardiac output.
At high doses dopamine has alpha 1 activity and causes
vasoconstriction. Dobutamine stimulates the beta 1
receptors in the myocardium and improves contractility
and increases heart rate. Precursor to epinephrine and
norepinephrine; stimulates the dopamine 1 receptors
and causes vasodilation; when moderate doses are
given, it stimulates the beta 1 receptors and improves
contractility and cardiac output. High doses has alpha
1 effects causing vasoconstriction.
d. Describe pathologic and physiologic factors which increase or decrease
myocardial contraction.
Factors which Increase Cardiac Factors which Decrease Cardiac
Contraction Contraction
Catecholamines-increase the activity of Beta blockers-block the effect of the
the calcium pump in the sarcoplasmic catecholamines
reticulum; therefore, it increase the
release of calcium from SR
Increases in the intracellular calcium Heart failure with systolic dysfunction
Decrease extracellular sodium-decreases Acidosis
the activity of Na/Ca exchanger
Digitalis-blocks the Na/K pump which Hypoxia/hypercapnia
increases the intracellular Na, decreases
the activity of the Na/Ca exchanger, and
, increases the intracellular Ca
Nondihydropyridine calcium channel
blockers (Diltiazem, Verapamil)
e. Describe how diltiazem, verapamil, digitalis, beta blockers and dobutamine affect
myocardial contraction.
Medication Increases or decreases How does it increase or Clinical Implications
contraction decrease contraction?
Diltiazem & Decreases They inhibit the influx These medication
Verapamil of calcium into the should be avoided in
myocardium. This persons with systolic
decreases the heart failure. Helpful
intracellular calcium for HTN, prinzmetal
concentration which in angina
turn decreases the
myocardial tension and
contractility. They have
negative inotrophic
effects.
Vasodilation= decrease
BP, decrease
SVR=decrease afterload
Digitalis Increases
Beta Blockers Decreases
Dobutamine Increases; increases HR Synthetic
(chronotrophy) and catecholamine, direct
lowers the afterload beta 1 agonist and some
beta 2 and alpha 1
effects
Beta 2 stimulation
causes vasodilation
(lower afterload)
Aging and the Cardiovascular System
1. Describe how the normal anatomy and physiology of the arteries and left ventricle are
altered by the aging process.
2. Explain the prenatal and post-natal development of the cardiovascular system.
3. Differentiate between the effects of aging on the anatomical and physiologic processes of
the cardiovascular system.
Cardiovascular Effects of aging
structure / Process
Cardiac Index: A slight decrease in the cardiac index for women while at rest.
During exercise the CI decreased for both genders because of
decrease in HR and stroke volume
Heart Rate The resting HR decreases but during exercise the increase in HR is
