Unit 7: Cardiovascular System
Blood
Blood represents about 8 percent of total body weight
Average volume
5 liters in females – haematocrit (formed elements in blood)42 percent
5.5 liters in males – haematocrit 45 percent, will have more RBC
Functions of Blood:
transport
Homeostatic regulation (pH, ion concentrations, body temperature)
Protection (clotting & immune protection)
Hematocrit
Percentage of blood occupied by cells
female normal range
38 - 46% (average of 42%)
male normal range
40 - 54% (average of 45%)
testosterone
Anemia
not enough RBCs or not enough hemoglobin
Hematocrit is too low
Polycythemia
too many RBCs (over 65%)
dehydration, tissue hypoxia, blood doping in athletes
Hematocrit is too high
Erythrocytes
Red blood cells (RBCs)
Trasport respiratory gases
Contain no nucleus, organelles, or ribosomes (they kick them out, they cannot make their own energy)
Biconcave discs
Provides larger surface area for diffusion of O2 across the membrane
Thinness of cell enables O2 to diffuse rapidly between the exterior and innermost regions of the cell
Lets them stack like plates to be able to move easily through small capillaries so clotting doesn't happen
Flexible membrane
Allows RBCs to travel through narrow capillaries without rupturing in the process
Contain hemoglobin
Normal RBC count
male 5.4 million/drop
female 4.8 million/drop
Hemoglobin
Pigment containing iron
Transport CO2 and O2
Appears reddish when oxygenated
Appears deep prple when deoxygenated
Molecule consists of two parts
Globin portion → proteins that are folded together
Protein composed of four highly folded polypeptide chains
Heme groups
Four iron-containing nonprotein groups
Each is bound to one of the polypeptides
Primary role is to carry O2 and CO2
Is reversible and easily broken, temporary
Also combines with
Carbon dioxide
Acidic hydrogen-ion portion (H+) of ionized carbonic acid
Carbon monoxide
Nitric oxide
Oxyhemoglobin: Hemoglobin (in red blood cells) bound to oxygen. This is the form of hemoglobin that carries oxygen from the lungs to the tissues.
Deoxyhemoglobin: Hemoglobin that has released its oxygen and is not bound to any. This form returns to the lungs to pick up more oxygen.
Carbaminohemoglobin: Hemoglobin bound to carbon dioxide. This form helps transport carbon dioxide (a waste product) from the tissues back to the lungs for exhalation.
Erythrocyte enzymes
Glycolytic enzymes
Because they lack organells they have a hard time creating energy so they rely on enzymes
Rely on glycolysis for ATP formation
Carbonic anhydrase
Critical in CO2 transport
Catalyzes reaction that leads to conversion of metabolically produced CO2 into bicarbonate ion (HCO3-) and water
Primary form in which CO2 is transported in blood, if CO2 is too high the body has strategies to replenish O2
Erythropoiesis: production of RBCs
Site:
prenatal-yolk sac, liver, spleen
postnatal bone marrow
From pluripotent (unspecialized blood cells)stem cells
Hormone → erythropoietin
Spleen removes old erythrocytes from circulation
Life cycle of a RBC
RBCs live only 120 days
No nucleus (no DNA) – no cell division (cant fix themselves)
Worn out cells removed by fixed macrophages in spleen & liver. “Heme” of hemoglobin can be recycled
Breakdown products are recycled
White blood cells
FUNCTION: help your body fight against pathogens
All WBCs (leukocytes) have a nucleus
Classified as granular or agranular based on presence of cytoplasmic granules
Leukocytes
Granulocytes and monocytes are produced only in bone marrow
Most new lymphocytes are actually produced by lymphocytes already in lymphoid tissues such as lymph nodes and tonsils
Total number of white cells and percentage of each type may vary considerably to meet changing defense needs
Leukocytes
NEUTROPHILS
Phagocytic specialists
Highly mobile
Attaching and digesting pathogens
Destroy bacteria by phagocytosis
Functions
First defenders on scene of bacterial invasion
Very important in inflammatory responses
Protective response
Prostiglandins - cause inflammation
Leucatrins- call in more WBC
Scavenge to clean up debris
EOSINOPHILS
Increase in circulating eosinophils (eosinophilia) is associated with
Allergic conditions such as asthma and hay fever
Internal parasite infestations, such as worms
Attach to parasite and secrete substances to kill it
BASOPHILS
Least numerous and most poorly understood of the leukocytes
Quite similar structurally and functionally to mast cells
Synthesize and store
Histamine (mast cells) – release is important in allergic reactions
Lymphocytes
Provide immune defense against targets for which they are specifically programmed
Live about 100 to 300 days
Two types of lymphocytes
B lymphocytes → turns into specialized plasma cells
Produce antibodies → recognize pathogens after you are exposed
Responsible to antibody-mediated or humoral immunity
T lymphocytes
Directly destroy specific target cells by releasing chemicals that punch holes in the victim cell (cell-mediated immunity)
Cytotoxins secrete perforin → lysis membrane of pathogen so it can get in
Target cells include body cells invaded by viruses and cancer cells
NK (Natural Killer) cells
Immune surveillance, cancer prevention
Monocytes
Emerge from bone marrow while immature and circulate before settling down in various tissues in body
Mature and enlarge in resident tissue and become known as macrophages (aggressive)
Life span can range from several months to years
leukopoiesis : formation of leukocytes/WBC
Clinical application:Medical uses of growth factor
Made using recombinant DNA technology
Erythropoietin (EPO) used for decreased RBC production of end-stage kidney disease. Made in liver and kidneys
Colony Stimulating Factors given to stimulate WBC formation in cancer patients receiving chemotherapy which kills bone marrow
Thrombopoietin helps prevent platelet depletion during chemotherapy, stimulates platele making
Terms to know:
Leukocytosis: An increase in the number of white blood cells (WBCs) in the blood, often due to infection or inflammation.
Leukopenia: A decrease in the number of white blood cells (WBCs) in the blood, which can make the body more vulnerable to infections.
Neutrophilia: An increase in the number of neutrophils (a type of white blood cell), usually in response to bacterial infection or inflammation.
Lymphocytosis: An increase in the number of lymphocytes (another type of white blood cell), often seen in viral infections.
Monocytosis: An increase in the number of monocytes (a type of white blood cell), typically in response to chronic infections or inflammation.
Platelet (thrombocytes)
Disc-shaped, 2 - 4 micron cell fragment with no nucleus
Normal platelet count is 150,000-500,000/cu mm of blood
average 350,000/cu mm
No nucleus, contains SER
Platelets form in bone marrow
Hormone - thrombopoietin produced by liver , stimulates production of platelets
Short life span (5 to 9 days in bloodstream)
Old platelets removed by fixed macrophages in liver and spleen
Functions of platelets
Platelet plug formation
Hemostasis: blood not moving = clotting
Steps in the process of blood clotting
platelet adhesion
platelet release reaction
platelet aggregation
Blood clotting process
Vascular phase (vascular spasm): muscle tightens and tries to pinch themselves closed to slow bleeding
Platelet phase (platelet aggregation, pinch and platelets do its job )
release chemicals like ADP, PAF, vWf (von Willebrand factor, call everyone to the site of injury)
Platelet adhesion/ platelets stick to exposed fibers
Coagulation phase (clot formation)
involve coagulation factors
coagulation cascade (a sequence of reaction)
Clot retraction
Clot destruction
Clotting cascade
Series of steps involving 12 plasma clotting factors that lead to final conversion of fibrinogen (meshwork that platelets can stick too) into a stabilized fibrin mesh
May be triggered by
Extrinsic pathway
Requires contact with tissue factors external to the blood
Tissue thromboplastin released from traumatized tissue directly activates factor X
Intrinsic pathway
Involves seven separate steps
Set off when factor XII (Hageman factor) is activated by coming into contact with exposed collagen in injured vessel or foreign surface such as glass test tube
Final common pathway
Prothrombinase and Ca+2:
catalyze the conversion of prothrombin to thrombin
Thrombin:
in the presence of Ca+2 converts soluble fibrinogen to insoluble fibrin threads
activates fibrin stabilizing factor XIII
Terms to know;
Prothrombin: A protein in blood that is converted into thrombin during clotting.
Thrombin: An enzyme that helps turn fibrinogen into fibrin, which forms a blood clot.
Fibrinogen: A protein in blood that gets turned into fibrin to help form blood clots.
Fibrin: A protein that forms a mesh-like structure to help stop bleeding by creating a blood clot.
Plasminogen: A protein in blood that, when activated, helps break down blood clots.
Plasmin: An enzyme that breaks down fibrin in clots, helping to dissolve them after they've done their job.
Clinical application
BLEEDING DISORDERS
Platelet problems
Too much bleeding
Thrombocytopenia → not enough platelets
von Willebrand’s disease → genetic
Clotting factor problems
Hemophilia → not able to clot properly
Liver diseases → clotting factors are made here so if liver is failing then they wont be made
INAPPROPRIATE CLOTTING
Thrombus → clot that is attached (fixed)
Abnormal intravascular clot attached to a vessel wall
Can eventually completely occlude the vessel
Too much clotting
Emboli → clot that has broken away (motile)
Freely floating clots
Can suddenly block blood flow
Inappropriate Clotting
Factors that can cause thromboembolism → obstruction of a blood vessel by a clot
Roughened vessel surfaces associated with atherosclerosis → hardening of the arteries
Imbalances in the clotting-anticlotting systems
Slow-moving blood → more likely to clot
Occasionally triggered by release of tissue thromboplastin into blood from large amounts of traumatized tissue
ABO Blood Group
Based on 2 glycolipid iso-antigens called A and B found on the surface of RBCs
Blood type is based on antigens on surface
Plasma contains isoantibodies or agglutinins to the A or B antigens not found in your blood
anti-A antibody reacts with antigen A; anti-B antibody reacts with antigen B
Rh blood group
Antigen was discovered in blood of Rhesus monkey
People with Rh agglutinogens on RBC surface are Rh+.
Normal plasma contains no anti-Rh antibodies; Antibodies develop only in Rh- blood type & only with exposure to the antigen
transfusion of positive blood; during a pregnancy with a positive blood type fetus
Clinical Application:
Blood transfusions reactions
Hemolytic disease of the newborn
Hemolytic disease of newborns \
Mom's body creates Rh antibodies with the first child (first pregnancy doesn't matter)
In 2nd child, hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs
RhoGAM → bind to antigens and makes it like nothing has happened, is the treatment)
Universal donors and recipients
People with type AB blood called “universal recipients” since have no antibodies in plasma
People with type O blood cell called “universal donors” since have no antigens on their cells
You shouldn't receive anything you don't already have
Lesson 2:Heart
Cardiovascular system
Includes the heart, blood, and blood vessels
Blood is a form of connective tissue
2 Circuits:
Pulmonary circuit- blood flows from the heart to the lungs
Systemic circuit- blood flows from the heart to the body
Functions of the cardiovascular system:
Deliver oxygen and nutrients to the tissues of the body
Remove CO2 and waste products
Location and orientation of the heart
The heart is located between the two lungs in the mediastinal space (esophagus and trachea are stabilizing tissues
Posterior to the sternum
Sits at an oblique angle, slightly rotated to the left
Is on an angle, rotated to the left which brings the apex forward a bit
Apical pulse: pulsation you can feel and hear if they are lying on left side
4 borders: superior, inferior, right and left
Base of heart forms (widest part)superior border (where great vessels attach)
RA forms right border
LV and LA form left border
RV forms inferior border (aka inferior surface)
Superficial anatomy of the heart
The atrial walls are very thin because they need to expand when blood is in them
Auricle of left atrium: a section of the atria that is able to stretch even more (extra stretchy)
Fat in anterior interventricular sulcus: runs between the two ventricles
Fat in coronary sulcus: filled with fat, protects the blood vessels and nerves. Between the atria and ventricle
The pericardium
The pericardium refers to the membranes surrounding the heart
The pericardium includes an outer fibrous layer and two serous layers.
Fibrous pericardium- fibrous connective tissue; stabilizes heart
Serous pericardium- consists of an outer parietal layer and inner visceral layer
Parietal pericardium
3 layers of tissue lining the fibrous pericardium (innermost layer is the mesothelium) is innermost for parietal
Visceral pericardium (aka epicardium)
2 layers of tissue that cover the surface of the heart outermost layer is the mesothelium) is outermost for visceral
Between the parietal and visceral pericardium is the pericardial cavity, which contains 15-20 mL of pericardial fluid
Cardiac tamponade: too much fluid in the pericardium, heart can't beat/expand
Pericarditis: infection that causes inflammation in the pericardial cavity. Heart can't beat cause cavity is swollen
The heart wall
Layers of the heart wall (from outside in):
Epicardium – external surface of the heart (this is the visceral pericardium)
Myocardium – cardiac muscle, connective tissue (including a fibrous skeleton), nerves. Thick muscly part
Endocardium – epithelium lining inner surface of the heart, including the valves also lines the valves
The heart muscles are arranged where they squeeze and twist. Different than skeletal muscles
The innermost layer continues into the veins of the heart
Internal anatomy of the heart
The heart has 4 chambers:
Right Atrium (RA)
RIght Ventricle (RV)
Left Atrium (LA)
Left Ventricle (LV)
The chambers are separated by septa
Interatrial septum; interventricular septum
The heart has 4 valves that direct the flow of blood between chambers and into vessels:
2 semilunar valves: pulmonary and aortic
2 atrioventricular (AV) valves: tricuspid valve (right atrium and right ventricle) and mitral (bicuspid) valve (left atrium and left ventricle)
Other important structures:
Chordae tendineae- fibrous tissue that allows for closure of valves and ensures proper positioning
Papillary muscles- skeletal type muscles that anchor the chordae tendineae
Cardiac skeleton: tough elastic tissue that wraps around the valves of the heart, providing stability and structure. Electrical insulation
Flow of blood through the heart
RA receives blood from the rest of the body via the inferior and superior vena cava
Blood travels through the tricuspid valve as it moves from the RA to the RV
From the RV, blood will pass through the pulmonary valve to the pulmonary trunk and arteries (for gas exchange at the lungs)
Blood returns to the heart through the pulmonary veins and enters the LA
From the LA, blood will pass through the mitral valve to the LV
From the LV, blood can be pumped to the rest of the body through the aortic valve and ascending aorta
Blood should only go one direction, the valves prevent blood from flowing backwards
Regurgitation of blood → blood going the wrong way
Stenotic valve → a very stiff valve, does not work
Rheumatic fever → over exaggeration reaction to a strep infection that damages heart
Overall function of the heart
The heart functions as two pumps that work simultaneously:
The right side of the heart receives deoxygenated (used) blood and pumps it to the lungs to be oxygenated
The left side of the heart receives oxygenated blood and pumps it to the entire body as well as the coronary arteries
Coronary blood supply
Remember:
The heart is specialized for pumping blood around the body, but it also requires its own supply of oxygen and nutrients in order to function.
Blood is supplied to the heart by the coronary circulation
Coronary arteries:
Originate within the aortic sinus at the base of the ascending aorta (pressure here is enormous to ensure blood supply to the heart)
Two major coronary arteries:
Right coronary artery – branches out to supply oxygenated blood to RA, RV, part of LA, part of LV, interatrial septum, part of interventricular septum and part of the conducting system of heart
Left coronary artery - branches out to supply oxygenated blood to LA, LV, parts of RV, parts of interventricular septum
Coronary Veins
Collects wastes from cardiac muscle
Drains deoxygenated blood into the coronary sinus (large vein) on posterior surface of heart; Coronary sinus empties into RA
Heart attack: the clot is not in the heart, it is a clot in a vessel in the coronary blood supply. The vessel clots and dies because of it
Conduction of impulses in the heart
Cardiac muscle tissue contracts in response to electrical impulses originating within the muscle tissue itself; this is referred to as autorhythmicity (heart muscle can contract on its own without stimulus from nerve fiber)
There are 2 types of cells involved in contraction of the heart muscle:
Specialized autorhythmic cells (pacemaker cells and conducting cells)
Contractile cells (99% of myocardial cells)
Pacemaker cells (aka nodal cells) are responsible for establishing heart rate.
Sinoatrial (SA) node: is the cardiac pacemaker, the primary driver of heart rate
Atrioventricular (AV) node: junction of atria, receives signal from SA node and sends message to rest of heart to contract. Is backup if anything happens to SA node
Ejection fraction: how much blood the heart is pushing out, fast pumping doesn't allow for sufficient blood to the body
Pacemaker cells
Sinoatrial (SA) Node:
Located in posterior wall of right atrium
Main pacemaker of the heart, where electrical impulses are generated
Generates action potentials at a rate of 60-100 per minute
Your heart will listen to the loudest voice and this one is
Heart rate= how many beats per minute
Heart rhythm= is it steady
Atrioventricular (AV) Node:
Located at the junction between the atria and ventricles
Sends the signal generated by the SA node forward to the rest of the heart
Generates action potentials at a rate of 40-60 per minute
→ leaky channels: Na+ leaks through so there is always a gradual push to threshold
→ pacemaker potential: membranes that is slowly making its way to action potential
Wave like contractions that help shove the blood in the right direction. From base of heart up and out of it
Pacemaker potential
There is no steady resting potential in these cells
Na+ slowly leaks into the cell
When threshold is met (-40mV), depolarization occurs and calcium channels open
Calcium rushes in, causing the rising phase
At peak, K+ channels open and K+ leaves the cell
Rapid repolarization caused by inactivation of Ca+ channels and activation of K+ channels
Electrical activity of heart
Atria contract as single unit followed after brief delay by a synchronized ventricular contraction
Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction
Ensures adequate ejection time
Plateau primarily due to activation of slow L-type Ca2+ channels, repolarization is slower to start
Because long refractory period (impossible to generate an action potential) occurs in conjunction with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible
Ensures alternate periods of contraction and relaxation which are essential for pumping blood
No tetanus in cardiac tissue because there is a plateau and a slow repolarization
Electrocardiogram (ECG)
An ECG is a reading of electrical currents (activity) generated by cardiac muscle during depolarization and repolarization
Different parts of the ECG record can be correlated with different cardiac events
There are many different leads that are used to see heart rate, lead 2 is the standard
Clinical considerations:
Abnormalities in Heart Rate:
Tachycardia- too fast
Rapid heart rate of more than 100 beats per minute
Bradycardia- too slow
Slow heart rate of fewer than 60 beats per minute
Abnormalities in Heart Rhythm:
Rhythm – regularity or spacing of ECG waves, miscommunication in the SA node
Arrhythmia – variation from normal rhythm and sequence of excitation of the heart, not a steady rhythm
Examples: atrial fibrillation, ventricular fibrillation, heart block
Ectopic pacemakers → some other conductive cell that send an action potential and mess with sinus rhythm
Asystole → no contraction of heart, no heart rhythm, can't use a defibrillator because there is no electrical current in the heart
Contractile cells
99% of myocardial cells
Action potential from pacemaker cells → contractile cells
Energy for contraction:
Aerobic metabolism in mitochondria, need O2 for contraction of heart
Oxygen obtained from coronary circulation and O2 stored on myoglobin
Reminder: myoglobin (protein that carries and stores oxygen in muscles) is a protein that stores oxygen in active muscles, found in the sarcoplasm
Supply of calcium in the sarcoplasmic reticulum (SR)
Direct communication via gap junctions
Long contractile plateau and refractory period
Summation and sustained contraction do not occur
Intercalated disks → special muscle cells that allow they heart to contract uniquely
Functional syncytium → function in synchronized way
Ca influx lengthens the action potential
As a result, cardiac muscle has a long refractory period because of the prolonged action potential
Cardiac Cycle
The heart cycles between periods of contraction and relaxation (alternating periods)
The period from the start of one contraction to the start of the next is referred to as one CARDIAC CYCLE
One cardiac cycle = one complete heartbeat
Caused by rhythmic changes in cardiac electrical activity and pressure
Cardiac cycle can be divided into periods of SYSTOLE and DIASTOLE
Systole- period of contraction; when a chamber contracts and blood is pushed into the next chamber or arterial vessel (pressure increases)
Diastole- period of relaxation —> refilling with blood. relaxation; period when chambers are filling with blood and preparing for the next contraction. Prepare for next contraction (pressure decreases)
Remember:
Fluids will move from an area of higher pressure to an area of lower pressure
Valves ensure that blood flows in the right direction
Terms to know:
End-Diastolic Volume (EDV): The amount of blood in the heart's ventricles at the end of filling (just before it contracts).
End-Systolic Volume (ESV): The amount of blood left in the ventricles after the heart contracts.
Ejection Fraction (EF): The percentage of blood pumped out of the ventricles with each heartbeat. It’s calculated as:
Stroke Volume (SV): The amount of blood the heart pumps out with each beat.
Isovolumetric Contraction: The phase of the heart's contraction when all heart valves are closed, and the ventricles contract without changing volume.
Isovolumetric Relaxation: The phase when the ventricles relax, but all valves are still closed, so no blood enters or leaves the heart.
Cardiac Output (CO): The total volume of blood the heart pumps per minute.
Cardiac cycle
Atrial Systole
Pressure increases in the atria and blood is pushed into ventricles through open AV valve (makes up last 30% of blood to fill ventricle)
The amount of blood in the ventricles at this point is the End-Diastolic Volume (EDV)
Ventricular Systole
Pressure rises in the ventricles and pushes the AV valves closed (S1 sound)
At this point, all valves are closed = isovolumetric contraction
Pressure continues to increase and semilunar valves open allowing for ventricular ejection
The amount of blood that leaves the ventricle is the Stroke Volume (SV)
The amount of blood left in the ventricle following ejection is the End-Systolic Volume (ESV)
Ventricular Diastole
Ventricular pressure decreases and blood from vessels pushes semilunar valves closed (S2 sound)
At this point, all valves are closed = isovolumetric relaxation (tension is reducing but the valves are still closed → atrial is filling up again)
When pressure of ventricles drops below that of the atria, the AV valves open and the cycle repeats
Blood passively fills into atria
Blood won't go back through valve because the blood wants to go high pressure (atria) to low pressure (ventricle(
Atrial systole, the AV valve opens
Then the pressure shifts and it higher in the ventricle than the atria so blood wants to move again and since it can't go back through the valves it is pushed up through the pulmonary trunk
Here is where we take end diastolic volume before the ventricle contacts. It's the total volume of blood that is in the heart.
As the blood goes up the pulmonary trunk to the pulmonary arteries is where we get isovolumetric volume from → pressure is high but not high enough to open semilunar valve
When the sweet spot is reached there will be enough pressure to open the bicuspid valve
The it is ventricle ejection
Anticipated EDV in a healthy adult= 130mL
Anticipated SV in a healthy adult= 70-80mL
Anticipated Ejection Fraction in a healthy adult= 60% (sustainable at 100% heart is dry and cannot refil)
Cardiac Output:
Refers to the amount of blood ejected from the left ventricle out of the heart in one minute
Cardiac Output (CO)= SV (mL) x Heart Rate (beats per minute)
Example: If an individual has a stroke volume of 75 mL and a heart rate of 80 beats per minute, what is their cardiac output?
CO=SV x HR → CO= 75 x 80 → CO= 6000mL/minute → CO= 6L/minute
Contractility → ability to contract
If low cardiac output weak, tired, fainting
Autonomic tone → heart never fully relaxes
Venous return: how much is filling the atria
Preload, afterload, contractility
Preload:
the degree of stretch in ventricles during diastole
Directly proportional to EDV
Amount of blood to be ejected; dependent on venous return
How well blood is being retured to the heart from the body
How stretched the ventricles
Afterload:
The pressure that the heart must pump against; the tension needed in the ventricle to open the semilunar valves and push blood out
Anything (peripheral rethat increases resistance in peripheral blood flow will increase afterload
Amount of pressure
Contractility:
Frank Starling Law → The greater the heart has ro overcome muscle is stretched during filling, the greater the force of contraction and the greater the quantity of blood pumped into the aorta
Within physiological limits
Heart sounds
Stethoscope
Sounds of heartbeat are from turbulence in blood flow caused by valve closure
first heart sound (lub or S1) is created with the closing of the atrioventricular valves (start of ventricular contraction)
second heart sound (dub or S2) is created with the closing of semilunar valves
Normal Heart Sounds, Lub (S1) Dub (S2)
Control of cardiac activity
ANS
Heart and greater vessels are highly innervated by cardiac plexus
Autonomic tone
SNS → norepinephrine and epinephrine
PNS → acetylcholine
Vagus nerve is responsible for most PNS innervation
Innervates SA & AV nodes
Chemoreceptors (O2 and CO2 kickstart reaction = heart needs to beat faster) in cardiac center of medulla
Baroreceptors in aortic & carotid sinuses → pressure increases heart rate
Atrial stretch (Bainbridge Reflex): atrial reflex increases in heart rate, increased preload = increased heart rate
Thyroid hormones→ metabolic activity, elevated T3 and T4 = Increased heart rate, mimics SNS
And many more…
→ heart failure: chronic progressive condition. Heart muscle cannot efficiently pump blood, fluid builds up around the lungs (left side of the heart) and rest of body (right side of heart). Blood flow between heart and other tissues is insufficient
Unit 7: Lesson 3- Blood Vessels & Circulation
What is interstitial fluid ?
All of the fluid between the blood vessels and cells
Consists of water, nutrients (amino acids, sugars, fatty acids, salts, ect), hormones, enzymes, waste products…
The interchange of things have to go through the interstitial fluid
Following Blood Flow from the Heart to the Heart
Blood Vessels
Need to be resilient and flexible
Resilient to withstand pressure and pressure changes as Blood moves through them
Flexibility to accommodate other tissues around them
Terms to Know:
Anastomosis: the joining of two vessels; a connection between to peripheral vessels (w/o and intervening capillary bed→ bypasses something else and is outside capillary bed)
Collateral: more than one artery supplying an area (Backup vessels → small, not used much)
Angiogenesis: the formation of new blood vessels; controlled by vascular endothelial growth factor (VEGF)
Five types of Blood Vessels
Artery- Blood vessels that carry blood away from the heart and toward a peripheral capillary, highest pressure vessel, contains alot of elastin fibers
Arteriole- A small arterial branch that delivers blood to a capillary network
Capillary (Smallest)- A small blood vessel, located between an arteriole and a venule, whose thin walls allow for the diffusion of gasses, nutrients, and waste between plasma and interstitial fluid (microscopic exchange vessels)
Venule (Tiny vein)- Thin walled vein that receives blood from capillaries; venules unite to form a larger vein
Vein (Largest in diameter/lumen)- a blood vessel carrying blood from a capillary bed toward the heart, contains valves (Lumen- inner passageway through)
Distinguishing Arteries from Veins
Most arteries and veins run parallel to eachother (arteries → away, veins → too)
Walls of arteries are thicker than veins
Arteries maintain their circular shape (bc it has muscle) and veins typically collapse when cut
Endothelial lining of arteries have pleated floods → endothelial lining of veins do not
Blood Vessel Walls
Vessel walls have three layers, blood vessels exist on a continuum with histology changing depending on location
Tunica Intima
Endothelium
Composed of simple squamous epithelium (really good at diffusion) & thin layer of connective tissue with elastic fibers
If arteries contract, the endothelium does not move → creates folds
Tunica Media
Composed of elastic fibers & sheets of smooth muscle tissue which cause vasoconstriction and vasodilation
Thickest layer (thicker in arteries, providing circular structure while veins collapse earlier)
Tunica Externa
Outermost layer, composed of connective tissue with elastic fibers
Anchor vessel to surrounding tissue
They blend into surrounding tissue
Arteries
Are generally thicker, can change in diameter actively from ANS or passively by blood flow
Elastic Arteries- The largest arteries; transport blood away from the heart. These Arteries are rich in elastic fibers and relatively few smooth muscle fibers. This enables resilience to high pressures and to decreasing pressures
Muscular Arteries- The medium arteries; thicker tunica media (more smooth muscle) , allowing for vasoconstriction and vasodilation, some are very superficial makes it important for pressure (superficial arteries are where you find a pulse) ex. Brachial, femoral
Arterioles- Small arteries carrying blood from muscular arteries to the capillaries; media has much less smooth muscle and less substantial adventitia. Arterioles branch into metarterioles which connect to capillaries (poorly defined outerlayer), referred to as RESISTANCE VESSELS
Vasodilation & Vasoconstriction
Vasodilation- an increase in the diameter of arterioles due to relaxation of smooth muscle in tunica media, decrease amount of resistance
Vasoconstriction- a reduction in the diameter of arterioles due to the contraction of smooth muscles in the tunica media, increase amount of peripheral resistance = more pressure
Occur in response to local factores; hormones, stimulation of vasomotor center (In medulla oblongata, control of vascular tone)
Will impact afterload (resistance that heart has to overcome to pump blood out → peripheral resistance increases afterload), peripheral blood pressure, and capillary blood flow,
Capillaries
MAJOR FUNCTION: Exchange vessels; smallest diameter
Single layer of simple squamous epithelium (endothelial tube) surrounded by a basement membrane
Found throughout body (except in avascular tissue), more extensively in highly active tissues (ex,muscles, brain, kidneys, liver)
3 types of Capillaries:
Continuous- standard, endothelial tube (is a continuous tube, no gaps between cells) with a basement membrane, no middle and outer layer. Water, small solutes, lipids travel through it, they hold blood and water inside
Fenestrated- has pores in the membrane “windows” through endothelial tissue. Hypothalamus, GI tract, choroid plexus (where CSF is produced)
Sinusoid- discontinuous endothelial cells and a broken basement membrane, blood moves through slowly, liver, bone marrow, spleen, adrenal and pituitary gland, transfer of plasma proteins
Capillary Bed
A interconnected network of capillaries, where diffusion occurs
Network of capillaries connecting metarterioles to venules
The opening of each capillary has a precapillary sphincter ( contract + relax a bunch and blood with be diverted, close of passageway → controls arterial blood flow in vessels, control amount of blood flow through the capillary)
Precapillary sphincter contracts (constricts) and relaxes (dialtes) several times a minute so that blood flows through in a pulsing fashion (controlled at tissue level autoregulation)
Capillary Exchange
All Chemical and gaseous exchange happens at the capillary level and is known as capillary exchange
Vital to homeostasis
Exchange between the blood and interstitial fluid → cells
Deliver nutrients and wastes, O2 and CO2 are exchanged across walls of capillaries
Close proximity to cells allows for rapid delivery
Materials move across capillary walls by:
Diffusion: need a concentration gradient, the net movement of ions from higher to lower concentration, down concentration gradient, Via channels (gaps in endothelium), fenestrated capillaries, sinusoid capillaries, plasma proteins can only diffuse over sinusoid vessels or else they will just stay in the blood
Filtration: hydrostatic pressure (the pressure exerted by the fluid in the capillaries, pushing solutes and solvent into interstitial fluid →cells), the removal of solutes as a solution flows across a porous membrane
Reabsorption: osmosis, as a result of osmosis (the diffusion of water across a selectively permeable membrane) Bulk flow→ hoe filtration and reabsorption work together as one that is continuous
Venules
Venules are the smallest veins
Carry blood from capillaries to larger veins
Tend to lack media (muscle layer, so no smooth muscle tissue) except in the larger venules
Veins
Medium sized veins- tunica media is thin with relatively few smooth muscle fibers; thickest layer is adventitia (tunica externa)
Large veins- superior and inferior vena cava, all three layers are thickest in the large veins
Low pressure system- 10% pressure of arteries (10% of pressure it started with, the pressure drops and is too low to withstand gravity, we rely on muscles + valves in extremities to move blood back), blood pre4ssure to low to overcome gravity so the intima in these veins have thin folds forming venous valves to prevent backflow of blood
Blood is also moved toward the heart by skeletal muscle
Venous valves
Compartmentalize blood flow
Eliminate backflow in low pressure system
Skeletal muscle movements push valves open
No movement = no blood flow, when you are sleeping you arnt fighting gravity
The Distribution of Blood
Distrobution of blood volume throughout vessels: 30-35% in arteries, capillaries, heart : 65-70% in veins (venus system → ⅓ of venous blood in liver, bone marrow and skin)
Veins are more distensible than arteries (veins are the reservoir of the blood)
Thinner walls, less muscular → able to expand 8x as much as parallel artery
Act as blood reservoir
Capacitance: relation between volume of vessels + pressure, can handle stress and large amounts of blood flow
Tissue Perfusion
Refers to adequate blood flow to the tissues, ensuring that the needs for oxygen and nutrients are being met.
Impacted by cardiac output, peripheral resistance, and blood pressure
When tissues are active, circulation must increase to meet demands
Vasomotion- Increase or decrease diameter of blood vessels, autoregulation, work together to meet demands of active tissue
Blood Flow
Adequate blood flow is needed to ensure adequate perfusion of tissues (oxygen supply)
Under normal conditions, blood flow mirrors cardiac output (CO= HRxSV, decrease CO = decrease capillary blood flow)
Capillary blood flow depends on pressure and resistance, is proportional
Pressure and resistance
Pressure- Generated by the heart to overcome resistance, absolute pressure is less important than pressure gradient
Pressure Gradient- the difference in pressure from one end of a vessel to the other, blood will flow from an area of higher pressure to an area of lower pressure
Resistance
flow - is proportional to the pressure gradient divided by the resistance
Arterial Blood Pressure
Blood pressure (BP) generated by the heart muscle must be enough to overcome the resistance present in the blood vessels (vascular resistance; peripheral resistance)
BP is the force exerted by blood against a vessel wall
Blood pressure:
Systolic blood pressure (SBP)
Peak pressure exerted by ejected blood against vessel walls during cardiac systole
Average= 120 mmHg (Systolic pressure @ ventricular systole)
Diastolic blood pressure (DBP)
Minimum pressure in arteries when blood is b=drained off into vessels downstream
Average = 80mmHG (diastolic pressure @ ventricular diastole)
Blood Pressure
BP= 120/80 mmHg → the peak pressure that is being exerted on vessels during peak pressure of heart, when it is squeezing
SBP > 140mmHg = hypertension (tension in the vessels)
SBP < 90mmHg = hypotension
Hypertension increases afterload, which will decrease CO overtime
Pulse pressure
How hard the heart has to work
Refers to the difference between SBP and DBP; measures strength of pulse wave
If BP is 120/80, pulse pressure =m 40mmHg
Mean Arterial Pressure
Refers to the everage arterial pressure through one cardiac cycle; used to calculate overall blood floe and as indicator of perfusion
MAP = DBP + ⅓ pulse pressure
In an adult, MAO should be a minimum of 65 mmHg
Factors Affecting Blood Pressure
Cardiac output
Resistance
Resistance to the flow of blood through small vessels is called total peripheral resistance
Peripheral resistance is determined by: i) blood viscosity ii) blood vessel length iii) blood vessel diameter (vasoconstriction, vasodilation)
The more viscous, longer, smaller the vessel is the more resistance there will be
Resistance
Total peripheral resistance- impacted by vascular resistance, viscosity, and turbulence
Vascular resistance- determined by friction (friction between blood and vessel wall, impacted by vessel length (more time blood has to slow down) and diametre ( smaller= more friction))
Viscosity- will be constant in the absence of compostation or disease, thinner blood = less resistance, too much hematocrit = thicker blood
Turbulence- altered blood flow due to turbulent/”swirling” flow, atherosterotic changes → hardening of arteries, narrowing of blood vessels due to too much junk in vessels
Arterioles
Major resistance vessels
Diameter of vessels supplying individual organs can be adjusted to distribute cardiac output and/or regulate arterial blood pressure
Mechanism involved in adjusting arteriolar resistance
Control of Blood Flow & Blood Pressure
Perfusion is the ability to provide adequate blood flow to meet tissue demands. Perfusion is impacted by cardiac output, blood pressure, and peripheral resistance
Primary determinants of blood pressure are cardiac output, and total peripheral resistance
Mechanisms to control blood flow and blood pressure are classified as: autoregulation (immediate, localized homeostasis adjustments), central regulation ( when autoregulation isn't working/ enough so it has to help, neural and endocrine mechanisms)
Autoregulation
Mechanisms that cause immediate, localized homeostatic adjustments
Vasodilation and constriction
Precapillary sphincters - dilation of precapillary sphincters is called vasomotion
Local vasodilators that may cause dilation of precapillary sphincters include low O2 or elevated CO2 , Nitric oxide (NO) from endothelial cells, inflammatory mediators, and increased tissue temperature.
○ Vasoconstriction
○ E.g. vessel injury causes endothelin release, which stimulates vascular spasm and platelet aggregation → vasoconstriction
○ Prostaglandins
If autoregulation is not sufficient, central regulation (neural and endocrine mechanisms) is called into action
Central Regulation Overview
1. Nervous System (Neural) Control
a. Cardiovascular centers in the medulla
i. Cardiac Center
ii. Vasomotor Center
b. Reflex Control
i. Baroreceptors
ii. Chemoreceptors
2. Endocrine System Control
a. Adrenal medulla- Norepinephrine and epinephrine
b. ADH
c. Aldosterone
d. Angiotensin II
e. Erythropoietin (EPO)
f. Natriuretic Peptides
Neural mechanisms
Sense change in arterial pressure or blood gas levels at specific locations and adjust cardiac output and peripheral resistance to maintain blood flow to vital organs
Cardiovascular (CV) centers of the medulla oblongata
Cardiac centers
Cardioacceleration (speed HR up = cardiac output ⬆) center (sympathetic activation) and cardioinhibitory center (Decrease HR)(parasympathetic activation)
Vasomotor Centre
Directs vasomotor responses in blood vessels; sympathetic input
Responsible for maintaining vasomotor tone at all times
Ex: adrenergic neurons secrete NE, which stimulates smooth muscle contraction → vasoconstriction (always active)
ex:Dilation of vessels in skeletal muscles (a more peripheral dilation) when Ach at neuromuscular junction stimulates NO synthesis (vasodilators)
Reflex control via baroreceptors & chemoreceptor
Baroreceptors
Located in carotid sinus (internal carotid artery), aortic arch, and wall of right atrium
Monitor for stretch (related to changes in BP) and communicate with CV center in brain to alter blood pressure
When BP ⬆, baroreceptor activity ⬆, leading to ⬇ CO and widespread peripheral vasodilation (due to activation of ANS)
When BP⬇, baroreceptor activity ⬇, leading to ⬆ CO and vasoconstriction (due to activation of ANS)
Parasympathetic inhibits sympathetic so body can calm down
Neural Mechanisms
Reflex control via Baroreceptors & Chemorecptors
Chemoreceptor reflex
Chemoreceptors are sensitive to the chemical composition and pH of fluids
Composition of arterial blood monitored by sensory neurons in carotid and aortic bodies; composition of CSF monitored by special receptors in the medulla
Requires coordination of cardiovascular and respiratory activities
⬆in the CO2 ( or ⬇ in O2 or pH) → stimulation of cardioacceleratory and vasomotor centers ⬆HR, ⬆CO, ⬆BP. Stimulation of respiratory center in medulla ⬆ respiratory rate and O2 intake
Endocrine Mechanisms
Hormones enhance short-term neural changes and direct long-term changes
Adrenal Medulla: stimulate by SNS → Epinephrine and Norepinephrine (NE) stimulate increase HR (increased CO) and vasoconstriction
Antidiuretic Hormone (ADH): released from posterior pituitary in response to decreased BP, ⬆ solute concentration, or ⬆ angiotensin II, stimulates conservation of water by kidney → elevate BP
Aldosterone: Released from adrenal cortex in response to low Na+ levels or ⬆ angiotensin II, stimulates conservation of Na+ → ⬆BP
Angiotensin II: in response to ⬇blood flow (⬇BP) to kidneys, kidneys release renin, which starts a chain reaction
Renin (inactive) converts inactive=ve angiotensinogen to angiotensin I (inactive) → Angiotensin-Converting Enzyme (ACE) converts angiotensin I to angiotensin II (active)
Function of angiotensin; stimulate aldosterone secretion (Na+ conservation), stimulates ADH secretion (water conservation), stimulates thirst, stimulates ⬆CO, stimulates vasoconstriction
Erythropoietin (EPO): Stimulates RB production, released by kidneys in response to low BP or low O2 levels, acts on blood vessels to cause vasoconstriction; stimulates RBC production → ⬆ O2 capacity
Natriuretic Peptides (opposite of angiotensin)
Released by myocardial cells in response to excessive cardiac stretch (BP to high, vessels to small)
Functions of Natriuretic peptides: stimulate Na+ and water loss by kidneys → ⬇ BP, inhibit hormones responsible for ⬆BP, inhibits thirst, stimulates vasodilation
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)
Works to ⬇ BP
Abnormalities in Blood Pressure
Hypertension- BP above 140/90mmHg
2 types of: primary hypertension, secondary hypertension
Primary hypertension: cause is typically unknown (bunch of little things), dietary factors, family history, lifestyle behaviors
Secondary hypertension: accounts for about 10% pf hypertension cases; occurs secondary to another known primary problem, ex) renal hypertension, endocrine hypertension
Hypotension- BP below 100/60 mmHg
Occurs when: there is too little blood to fill the vessels, heart is too weal to drive the blood, medication
Orthostatic (postural) hypotension; transient hypotensive condition resulting fron insufficient compensatory responses to gravitational shifts in blood when person moves from horizontal to vertical position (standing up and you get all dizzy, BP dips during sudden position changes)
Edema
An abnormal ⬆in interstitial fluid that can occur if filtration (fluid leaving capillaries) exceeds reabsorption (fluid moving into capillaries) SWELLING!! → capillaries are leaking, lymphatic vessels are not picking up substances
Excess filtration may be due to: hypertension (hydrostatic pressure, more fluid pushed out)
Inadequate reabsorption may be due to : decrease plasma proteins
Map of the circulatory System
Pulmonary circuit:
As blood leaves the right ventricle, it exits via the pulmonary trunk which branches into the left and right pulmonary arteries (carrying deoxygenated
blood toward the lungs)
Oxygenated blood returning from the lungs to the heart does so via pulmonary veins which empty into the left atrium.
NOTE: the pulmonary circuit is the only time arteries carry deoxygenatedblood while veins carry oxygenated blood!!!
FIGURE 21-17
Systemic circuit:
As oxygenated blood leaves the left ventricle, it does so via the ascending aorta. The left and right coronary arteries branch off the ascending aorta.
The ascending aorta curves into the aortic arch, from which the brachiocephalic trunk (on the right), left common carotid, and left subclavian arteries arise. The brachiocephalic trunk divides into the right common carotid and the right subclavian artery.
The descending aorta gives rise to the thoracic aorta and the abdominal aorta.
The abdominal aorta eventually branches into the left and right iliac arteries.
Right subclavian artery\
Location: just below the clavicle, upper chest
Taking blood to: right arm , shoulder and neck
Taking blood from: brachiocephalic trunk
Brachiocephalic trunk artery
Location: upper right side of your chest, above your heart and below your neck
Taking blood to: right side of head, neck, right arm ,chest
Taking blood from: aortic arch
Ascending aorta artery
Location: atop the left ventricle on the left side of your heart
Taking blood to: upper arm, forearm, hand
Taking blood from: subclavian artery
Brachial artery
Location: starts in your upper arm, just belwo your shoulder, and runs down through the crease in front of your elbow
Taking blood to:
Taking blood from:
Radial artery
Location: on the inside of the forearm from the elbow to the thumb
Taking blood to: forearm, wrist, hand
Taking blood from: brachial artery
Right common carotid artery
Location: in your neck, brachiocephalic trunk
Taking blood to: head, neck, and brain
Taking blood from: brachiocephalic trunk
Left common Carotid artery
Location:arises from your aortic arch, and is located in the neck and chest
Taking blood to: head, neck and brain
Taking blood from: aortic arch
Left Subclavian artery
Location: in the neck, below your collarbone, and originates from the aortic arch/ upper chest
Taking blood to: left arm, shoulder ,neck
Taking blood from: aortic arch
Descending Aorta artery
Location: in the chest and abdomen, beginning at the end of the aortic arch amd ending near the belly button (starts at the aortic arch)
Taking blood to: chest, lungs, abdomen, lower body
Taking blood from: aortic arch
Internal Carotid artery
Location: begin at the carotid bifurcation on either side of your neck
Taking blood to: brain, eyes, face scalp
Taking blood from: common carotid artery
Carotid Sinus artery
Location: at the base of the internal carotid artery, just above where the common carotid artery splits into the internal and external carotid arteries
Taking blood to: baroreceptors
Taking blood from: common carotid artery
Superficial temporal artery
Location: starts below your ear and runs vertically between your cheekbone and your ear
Taking blood to: scalp, temporal region, external ear
Taking blood from: external carotid artery
External Carotid artery
Location: on either side of the neck, traveling up towards the ear
Taking blood to: heart and neck
Taking blood from: the common carotid artery
Thoracic Aorta artery
Location: in the chest , from the aortic arch to the diaphragm
Taking blood to: diaphragm, upper body, chest and lungs
Taking blood from: heart/left ventricle
Inferior phrenic artery
Location: around the posterior aspect of the inferior vena cava and continues along the right margin of the vena caval foramen/ upper abdomen
Taking blood to: diaphragm, adrenal glands
Taking blood from: abdominal aorta
Renal artery
Location: abdomen
Taking blood to: the kidneys
Taking blood from: abdominal aorta
Common Iliac artery
Location: pelvic region
Taking blood to: pelvic region and lower limbs
Taking blood from:abdominal aorta
Celiac Trunk artery
Location: upper abdomen
Taking blood to: stomach, spleen, liver (through respective arteries)
Taking blood from: abdominal aorta
Dorsalis Pedis artery
Location: on top of the foot
Taking blood to: the foot
Taking blood from: tibial artery. Popliteal artery
Abdominal aorta artery
Location: beings in the lower part of chest, continuation of aorta
Taking blood to: abdominal organs
Taking blood from: left ventrical of heart
Posterior Tibial artery
Location: originates at the popliteal artery behind the knee, runs down the leg
Taking blood to: posterior compartment of leg
Taking blood from: popliteal artery
Popliteal artery
Location: popliteal fossa (depression in knee cap)
Taking blood to: knee joint, and muscles/tissues in the lower leg
Taking blood from: femoral artery
Femoral artery
Location: thigh
Taking blood to: lower limbs
Taking blood from: common/external iliac artery
Superior vena cava vein
Location: upper chest and mediastinum
Taking blood to: right atrium
Taking blood from: upper half of body
Inferior vena Cava vein
Location: in the chest below the heart (around L5)
Taking blood to: right atrium of heart
Taking blood from: lower half of body
External Jugular
Location: side of neck, superficially just under the skin
Taking blood to: the subclavian vein
Taking blood from: the face, scapl and parotid gland
Internal Jugular vein
Location: in the neck, running from the base of the skull to the upper chest
Taking blood to: the right atrium of the heart
Taking blood from: the brain, superficial reigions of the face and neck
What ar4e the 3 main branches of the aortic arch? What areas of the body are supplied by these vessels?
Effects of Aging on the Cardiovascular System
Age-related changes can be seen in the blood, heart, and blood vessels
Decreased hematocrit; increased risk of clots; increased pooling of blood in legs due to venous valve deterioration
Reduced CO; increased incidence of alterations in conduction
Reduced elasticity; increased incidence of atherosclerosis; increased risk of clots
Fetal circulation
Foramen Ovale- flap like opening in the interatrial septum,, bypasses lungs from one atria to another
Ductus Arteriosus- no blood to pulmonary trunk, blood that troes to go this way gets pushed back the other way
2 Umbilical arteries (back to placenta from fetus) and 1 umbilical vein (from placenta to fetus)
In adulthood: FOssa Ovalis, ligamentum arteriosum
Before birth fetal lungs are collapsed, digestive tract is not used yet → placenta is in charge