Study Guide Quiz 7 Exam 3 Cardiovascular System
1. Layers of Cardiac Tissue
a. Pericardium – fibrous covering around the heart
i. Fixed position in the thorax
ii. Physical protection against infection
iii. Disorders of the Pericardium
1. Pericardial effusion - presence of exudate in the pericardial cavity
2. Acute pericarditis - chest pain, ECG changes, and a friction rub
a. Causes: infections, uremia, rheumatic fever, connective tissue
diseases, MI
3. Chronic pericarditis - increase in inflammatory exudate that continues
beyond the acute period
4. Constrictive pericarditis - scar tissue between visceral and parietal layers
of the serous pericardium
b. Myocardium – muscular portion of the heart
i. Forms the walls of the atria and the ventricles
c. Endocardium – thin 3-layered membrane that lines the heart and covers the valves
2. Pulmonary v. Systemic Circulation
a. Pulmonary circulation
i. Right heart, pulmonary arteries, pulmonary capillaries, and pulmonary veins
ii. Moves blood through the lungs
iii. Link between gas exchange function of the lungs and systemic circulation
b. Systemic Circulation
i. Moves blood out of the heart through the aorta and distributes it to the periphery
3. Cardiac Cycle
a. Systole
i. Contraction passes from AV node to Purkinje fibers and ventricular cells
ii. Ventricles contract
iii. AV valves close
iv. SL valves open
v. Blood is pumped from ventricles to arteries
b. Diastole
i. Early diastole
1. Ventricles relax
2. SL valves close
3. AV valves open
4. Ventricles fill with blood
ii. Mid-diastole
1. Atria and ventricles are relaxed
2. SL valves are closed
, 3. AV valves are open
4. Ventricles continue to fill with blood
iii. Late diastole
1. SA nodes contract
2. Atria contract
3. Ventricles fill with more blood
4. Contraction reaches AV node
4. Preload v. Afterload
a. Preload – represents volume
i. Initial stretching of the cardiac cells prior to contraction
ii. Amount of blood the heart must pump with every beat
b. Afterload – pressure or tension work of the heart
i. Used to mean the tension produced by a chamber of the heart in order to
contract
5. Definitions
a. Cardiac contractility
i. Ability of the heart to change its force of contraction
ii. Inotropic drugs – influence the force of cardiac contraction
b. Heart rate
i. Number of contractions of the heart in one minute
ii. Chronotropic drugs influence the number of times the heart beats
1. Ex. Diltiazem, calcium channel blockers
c. Blood pressure
i. Blood pressure = cardiac output x peripheral resistance
d. Cardiac output
i. Cardiac output = stroke volume x heart rate
1. NL = 3.5-9 liters/min
e. Stroke volume
i. The volume of blood pumped from one ventricle of the heart with each beat
6. Diagnostic Tests
a. EKG
i. Gives information on heart rate and rhythm (electrical activity)
b. Echo
i. Ultrasound exam
1. Examines anatomy, structures, and function
c. Cardiac Catheterization
, Fluoroscopy to examine structure and function
i.
Best diagnostic test to rule out infarction
ii.
Rules out risk of clot or occlusion
iii.
Ablation
iv.
d. Electrophysiology study
i. Maps the electrical system
7. Artery Structure
a. Tunica intima - endothelium
b. Tunica media - smooth muscle
c. Tunica adventitia - collagen and elastic fibers
8. Atherosclerosis
a. Form of arteriosclerosis in which soft deposits of intra-arterial fat and fibrin on the vessel
walls harden over time
i. Can have partial or total occlusion
ii. Intermediate density lipoproteins -- IMPORTANT
b. Pathophysiology
i. Smooth muscle cells and collagen fibers migrate into the tunica intima, causing it
to stiffen and thicken, gradually narrowing the lumen
ii. Develops because scavenger cells encounter fatty deposits in the artery lining
1. Try to destroy the fats by oxidizing them
a. Oxidized fats injure the endothelium
b. Clots form and release growth factors
c. Smooth muscle grows over the fatty core
2. Try to remove the fats by eating them
a. Become “foam cells” in the core of the plaque
iii. Vessel injury occurs endothelial cell integrity is breached permeability of
endothelial cells to plasma components plasma cholesterol and fats gain access
to intima scar tissue replaces vascular wall cholesterol and fat build up, scar
tissue deposits, platelet-derived clots, smooth muscle cell proliferation diameter
of artery and stiffness
iv. Vessel injury occurs endothelial cell integrity is breached initiates inflammatory
and immune response stimulate smooth muscle cell proliferation, release of
vasoactive peptides and accumulation of macrophages and platelets platelet
aggregation, blood clots begin to form cholesterol and fat build up, scar tissue
deposits, platelet-derived clots, smooth muscle cell proliferation diameter of
artery and stiffness
c. Clinical Manifestations
i. Occur because of tissue ischemia and depend on which tissues are affected and
how long the ischemia lasts
1. Layers of Cardiac Tissue
a. Pericardium – fibrous covering around the heart
i. Fixed position in the thorax
ii. Physical protection against infection
iii. Disorders of the Pericardium
1. Pericardial effusion - presence of exudate in the pericardial cavity
2. Acute pericarditis - chest pain, ECG changes, and a friction rub
a. Causes: infections, uremia, rheumatic fever, connective tissue
diseases, MI
3. Chronic pericarditis - increase in inflammatory exudate that continues
beyond the acute period
4. Constrictive pericarditis - scar tissue between visceral and parietal layers
of the serous pericardium
b. Myocardium – muscular portion of the heart
i. Forms the walls of the atria and the ventricles
c. Endocardium – thin 3-layered membrane that lines the heart and covers the valves
2. Pulmonary v. Systemic Circulation
a. Pulmonary circulation
i. Right heart, pulmonary arteries, pulmonary capillaries, and pulmonary veins
ii. Moves blood through the lungs
iii. Link between gas exchange function of the lungs and systemic circulation
b. Systemic Circulation
i. Moves blood out of the heart through the aorta and distributes it to the periphery
3. Cardiac Cycle
a. Systole
i. Contraction passes from AV node to Purkinje fibers and ventricular cells
ii. Ventricles contract
iii. AV valves close
iv. SL valves open
v. Blood is pumped from ventricles to arteries
b. Diastole
i. Early diastole
1. Ventricles relax
2. SL valves close
3. AV valves open
4. Ventricles fill with blood
ii. Mid-diastole
1. Atria and ventricles are relaxed
2. SL valves are closed
, 3. AV valves are open
4. Ventricles continue to fill with blood
iii. Late diastole
1. SA nodes contract
2. Atria contract
3. Ventricles fill with more blood
4. Contraction reaches AV node
4. Preload v. Afterload
a. Preload – represents volume
i. Initial stretching of the cardiac cells prior to contraction
ii. Amount of blood the heart must pump with every beat
b. Afterload – pressure or tension work of the heart
i. Used to mean the tension produced by a chamber of the heart in order to
contract
5. Definitions
a. Cardiac contractility
i. Ability of the heart to change its force of contraction
ii. Inotropic drugs – influence the force of cardiac contraction
b. Heart rate
i. Number of contractions of the heart in one minute
ii. Chronotropic drugs influence the number of times the heart beats
1. Ex. Diltiazem, calcium channel blockers
c. Blood pressure
i. Blood pressure = cardiac output x peripheral resistance
d. Cardiac output
i. Cardiac output = stroke volume x heart rate
1. NL = 3.5-9 liters/min
e. Stroke volume
i. The volume of blood pumped from one ventricle of the heart with each beat
6. Diagnostic Tests
a. EKG
i. Gives information on heart rate and rhythm (electrical activity)
b. Echo
i. Ultrasound exam
1. Examines anatomy, structures, and function
c. Cardiac Catheterization
, Fluoroscopy to examine structure and function
i.
Best diagnostic test to rule out infarction
ii.
Rules out risk of clot or occlusion
iii.
Ablation
iv.
d. Electrophysiology study
i. Maps the electrical system
7. Artery Structure
a. Tunica intima - endothelium
b. Tunica media - smooth muscle
c. Tunica adventitia - collagen and elastic fibers
8. Atherosclerosis
a. Form of arteriosclerosis in which soft deposits of intra-arterial fat and fibrin on the vessel
walls harden over time
i. Can have partial or total occlusion
ii. Intermediate density lipoproteins -- IMPORTANT
b. Pathophysiology
i. Smooth muscle cells and collagen fibers migrate into the tunica intima, causing it
to stiffen and thicken, gradually narrowing the lumen
ii. Develops because scavenger cells encounter fatty deposits in the artery lining
1. Try to destroy the fats by oxidizing them
a. Oxidized fats injure the endothelium
b. Clots form and release growth factors
c. Smooth muscle grows over the fatty core
2. Try to remove the fats by eating them
a. Become “foam cells” in the core of the plaque
iii. Vessel injury occurs endothelial cell integrity is breached permeability of
endothelial cells to plasma components plasma cholesterol and fats gain access
to intima scar tissue replaces vascular wall cholesterol and fat build up, scar
tissue deposits, platelet-derived clots, smooth muscle cell proliferation diameter
of artery and stiffness
iv. Vessel injury occurs endothelial cell integrity is breached initiates inflammatory
and immune response stimulate smooth muscle cell proliferation, release of
vasoactive peptides and accumulation of macrophages and platelets platelet
aggregation, blood clots begin to form cholesterol and fat build up, scar tissue
deposits, platelet-derived clots, smooth muscle cell proliferation diameter of
artery and stiffness
c. Clinical Manifestations
i. Occur because of tissue ischemia and depend on which tissues are affected and
how long the ischemia lasts
