CARDIOVASCULAR SYS
CARDIOVASCULAR SYSTEM
Closed system of the heart and blood vessels
heart pumps blood
Blood vessels allow blood to circulate to all parts of the body
Function: deliver oxygen and nutrients and to remove carbon dioxide and other waste products
HEART
LOCATION
Thorax between the lungs
Apex: 5th Left ICS (Intercostal space) 3.5cm from the sternum
About the size of your fist
SURFACES OF THE HEART
Anterior (Sternocostal) Surface
Right Atrium, Right ventricle (most anterior part of the heart)
Inferior (Diaphragmatic)
Left ventricle, Apex of the heart, and right ventricle
Posterior (Base) Surface
Right atrium, left atrium (most posterior part of the heart)
COVERINGS
Pericardium
Visceral pericardium— next to heart
Parietal pericardium—outside layer
Serous fluid fills the space b/w the layers of pericardium
Pericardiocentesis: procedure that removes the excess pericardial fluid
LAYERS
Epicardium
Outside layer
Parietal pericardium
Connective tissue layer
Myocardium
Middle layer
Mostly cardiac muscle
Endocardium
Inner layer
endothelium
CHAMBERS
ATRIA
Receiving chambers
Receive from Superior and inferior vena cava
R & L
Separated by atrioventricular valves (tricuspid & mitral/bicuspid valve)
VENTRICLES
Discharging Chambers
R & L
VALVES
Allow blood to flow in one direction
Four valves
Atrioventricular valves—between atria and ventricles
Bicuspid valve (left)
Tricuspid (right)
Semilunar valves— between ventricle & artery
Pulmonary
Aortic valve
Valves open as blood is pumped through
Held in place by chordae tendineae (heart strings)
Close to prevent backflow
What happens if the valves do not close properly —> insufficiency, when ventricles contract there will be regurgitation of blood in the ventricles
Blood cannot pass through
Atria fills up
Atria will increase course of contraction (senotic something)
Atrial enlargement
GREAT VESSELS
Aorta: Leaves L. Ventricle
Pulmonary arteries: Leaves R. Ventricle
Vena cava: enters. R. Atrium
Pulmonary veins (4): Enter left atrium
PERICARDIUM
Location:
middle mediastinum
posterior to the body of the sternum and the 2nd to the 6th costal cartilages
anterior to the T5-T8
Fibrous Pericardium
Serous Pericardium
Parietal Layer
Visceral Layer/ Epicardium
Pericardial Cavity: slit like space between the parietal and visceral layers
contains 50 ml of tissue fluid
Pericardial fluid: acts as a lubricant to facilitate movements of the heart
Pericardial Sinuses
Oblique Sinus: a recess that forms from the large veins of the serous pericardium
Transverse Sinus: s a short passage that lies between the reflection of serous pericardium around the aorta and pulmonary trunk and the reflection around the large veins
Nerve supply: sympathetic trunks and vagus nerves
CORONARY CIRCULATION
Blood in the heart chambers does not nourish the myocardium
The blood that goes through does not supply the heart
The heart has its own nourishing circulatory system
Coronary arteries
cardiac veins
Blood empties in R. Atrium via the coronary sinus
Arterial Supply of the Heart:
Right Coronary Artery
Left Coronary Artery: supplies major part of the heart
Venous Drainage of the Heart: Coronary sinus
continuation of the great cardiac vein
CONDUCTION SYSTEM
Intrinsic conduction system (nodal system)
SA node
Internodal pathways (between the two nodes)
AV node
Bundle of his/AV bundle
L. & R branches
Purkinje Fibers
Heart muscle cells contract, without nerve impulses, in a regular continuous way
Contraction is initiated by the sinoatrial node
Sequential simulation occurs at other autorhythmic cells
Special tissue sets the pace
Sinoatrial node
Pacemaker
AV Node
Bundle of His
Purkinje fibers
CARDIAC CYCLE
Atria contract simultaneously
Atria relax, then ventricles contract
Systole=contraction
Diastole=relaxation
FILLING OF HEART CHAMBERS
Cardiac Cycle: events of one completes 1 heart beat
Mid to late diastole
blood flows into ventricles
ventricular filling
Atrial contraction
Ventricular systole
blood pressure builds before ventricle contracts, pushing out blood
isovolumetric contraction phase
Ventricular ejection phase
Atria in diastole
Ventricles are filled up and they need to contract to eject the blood
Early diastole
atria finish refilling, ventricular pressure is low
isovolumetric relaxation
chambers cannot contract all together
CARDIAC OUTPUT
CARDIAC OUTPUT (CO)
Amount of blood pumped by each side of the heart in one minute
CO= HR (Heart Rate) X SV (Stroke Volume)
Stroke volume: volume of blood pumped by each ventricle in one contraction
Related to blood pressure
Cardiac Output Regulation
REGULATION OF HEART RATE
Stroke volume usually remains relatively constant
STARLING’S LAW
the more that the cardiac muscle is stretched, the stronger the contraction
Changing heart rate is the most common way to change CO
INCREASED HEART RATE
Sympathetic NS
Crisis
Low blood pressure
Hormones
Epinephrine
Thyroxine
Beta Blockers are given—beta receptors respond to it
Increased thyroid hormones
Exercise
More demand from the heart
Muscles are being used
Decreased blood volume
Less circulating blood volume=less blood Going back to heart
Heart thinks it needs to go fast for the peripheral organ
There is a reason why there is low blood volume
Could be blood loss
Losses through vomiting or LBM (losses were not replaced
Other body systems will work to compensate for the loss (example: kidneys regulating ot conserve water because of water loss)
DECREASED HEART RATE
Parasympathetic NS
High blood pressure or blood volume
Decreased venous return
BLOOD VESSELS: THE VASCULAR SYSTEM
Arteries
Arterioles
Capillaries
Venules
Veins
ANATOMY
3 Layers (Tunics)
Tunic Intima (Interna)
Endothelium
Tunic Media
Smooth muscle
Controlled by sympathetic nervous system
Tunica Externa
Mostly fibrous connective tissue
DIFFERENCES BETWEEN BLOOD VESSEL TYPES
Walls of arteries are thickest
Lumens of veins are larger
Lumen: cavity within tubular structure
Skeletal muscle milks blood in veins toward the heart
Capillary beds
Walls of capillaries are only one cell layer thick to allow for changes between blood and tissue
Capillary beds: vascular shunt; true capillaries (exchange vessels)
MOVEMENT OF BLOOD THROUGH VESSELS
Most arterial blood is pumped by the heart
Veins use the milking action of muscles to help move blood
Capillary beds
Walls of capillaries are only one cell layer thick to allow for changes between blood and tissue
Capillary beds: vascular shunt; true capillaries (exchange vessels)
PULSE
Pressure of blood
Monitored at “pressure points” where pulse is easily palpated
PULSE POINTS
Temporal A.
Facial A.
Carotid A.
Brachial A.
Radial A.
Femoral A.
Popliteal A.
Posterior tibial A.
Dorsalis pedis A.
BLOOD PRESSURE
Measurements by health professionals are made on the pressure in large arteries
Systolic—pressure at the peak of ventricular contraction
Diastolic—pressure when ventricles relax
Pressure in blood vessels decreases as the distance away from the heart increases
Lower ex BP is different from upper ex BP
EFFECTS OF FACTORS
Neural factors
autonomic NS adjustments (sympathetic division)
Renal factors
Regulation by altering blood volume
Renin—hormonal control
Temperature
Heat—> vasodilation
Dako. ang lumen
Increased blood to the area
Promotes healing
Lactic acid accumulates
Blood washes away
Lactic is a by-product of lactic acid
Cold—> vasoconstriction
Chemicals
Various substances can cause increases or decreases
Example: propranolol
Diet
VARIATIONS IN BLOOD PRESSURE
Human normal range is variable
Normal BP
140-110 mm Hg systole
80-75 mm Hg systole
120/80
Hypotension
Low systolic (below 110 mm HG)
often associated w/ illness
Hypertension
High systolic (above 140 mm HG)
Can be dangerous if it is chronic
CAPILLARY EXCHANGE
Substances exchanged due to concentration gradients
Energy is not used
Passive because of the concentration gradient
Oxygen and nutrients leave the blood
Carbon dioxide and other wastes leave the cells
Diffuses through the capillaries
MECHANISMS
Direct diffusion across plasma membranes
Endocytosis or exocytosis
Some Capillaries have gaps (intercellular clefts)
Plasma membrane not joined by tight junctions
Fenestrations of some capillaries
Fenestrations=pores
DEVELOPMENTAL ASPECTS OF CARDIOVASCULAR SYSTEM
Simple tube heart develops in the embryo and pumps by the 4th week
Heart becomes 4 chambered organ by end of 7 weeks
Few structural changes occur afterward 7th week
BLOOD
only fluid tissue
Classified as a connective tissue
Living cells=formed elements
Non-living matrix=plasma membrane
PHYSICAL CHARACTERISTICS OF BLOOD
Oxygen rich–scarlet red
Oxygen poor--dull red
PH must remain b/w 7.35-7.45
Blood temp is slightly higher than body temp
Blood plasma—90% water
Nutrients
Salts (metal ions)
Respiratory gasses
Hormones
Proteins
BLOOD PLASMA
Plasma=55%
Water
Electrolytes
Salts
Plasma proteins
Albumin
IMMUNOGLOBULINS: ANTIBODIES
IGG
Increase if you had infection before
IGA
IGE
Immunoglobulin m
Increase circulating blood pag acute or recent infection
Immunoglobulin D
Denge: low WBC; platelet normal
Flu infection while recovering
PLASMA PROTEINS
Albumin: regulates osmotic pressure (protein that attracts water, water goes into the vessel)
Osmotic pressure: the blood that passes through the vessel it produces hydrostatic pressure;
Interstitial fluid: hydrostatic pressure pushes toward the vessel (SEE GEN PHYSIO NOTES)
NET FILTRATION PRESSURE
Clotting proteins: help to stem blood loss when a blood vessel is injured
Antibodies: help protect the body from antigens
FORMED ELEMENTS
Erythrocytes = RBC
Leukocytes= WBC
Platelets=cell fragments
ERYTHROCYTES (RED BLOOD CELLS)
Main function: carry oxygen
Anatomy of circulating erythrocytes
Biconcave disks
Essentially bags of hemoglobin
Anucleate (no nucleus)
Contains very few organelles
Outnumber white blood cells–1000:1
4-6 mil
Sacks of hemoglobin
Most organelles have been ejected
100-120 days
Checking 3 month compliance
More accurate than fasting blood sugar
Test: fasting blood sugar
HEMOGLOBIN
Iron-containing protein
Binds strongly, but reversibly, to oxygen
Each hemoglobin molecule has four oxygen binding sites
Each erythrocyte has 250 million hemoglobin molecules
Function: Transport oxygen bound to hemoglobin molecules; also transport small amount of carbon dioxide
LEUKOCYTES (WHITE BLOOD CELLS)
Crucial in the body’s defense against disease
These are complete cells, with a nucleus and organelles
Diapedesis: Able to move into and out of blood vessels
Can move by ameboid motion
Can respond to chemicals released by damaged tissues
LEUKOCYTE LEVELS IN THE BLOOD
Normal levels are between 4,000 and 11,000 cells per millimeter
Abnormal leukocyte levels
Leukocytosis
Leukopenia
Leukocytosis
Above 11,000 leukocytes/ml
Generally indicates an infection
Causes/ effects: leukemia
Leukopenia
Commonly caused by certain drugs
Complications: low immune system; dali makuha ng sakit
TYPES OF LEUKOCYTES
Granulocytes
Granules that can be seen in their cytoplasm
neutrophils, eosinophils, basophils
Neutrophils
Multilobed nucleus with fine granules
Act as phagocytes at active sites of infection
3000-7000
Eosinophils
Large brick-red cytoplasmic granules
Found in response to allergies and parasitic worms
100-400
Kill parasitic worms
Increase during allergy attacks
Might phagocytize antigen-antibody complexes and inactivate some inflammatory chemicals
Basophils
Have histamine-containing granules
Initiate inflammation
Agranulocytes
Lack visible cytoplasmic granules
Lymphocytes
Nucleus fills most of the cell
plays an important role in immune response
produces antibodies
T cells, b cells, NK cells
Monocytes
largest of WBC
function as macrophages–become macrophages in the tissues
important in fighting chronic infection
PLATELETS (THROMBOCYTES)
Derived from ruptured multinucleate cells (megakaryocytes)
Needed for clotting processes
Normal platelet count=300,000 mm^3
Hematopoiesis: Blood cell formation
occurs in red bone marrow
all blood cells are derived from a common stem cell (hemocytoblast)
Hemocytoblast differentiation
lymphoid stem cell produces lymphocytes
myeloid stem cell produces other formed elements
FATE OF ERYTHROCYTES
Unable to divide, grow, or synthesize proteins
Wear out in 100 to 120 days
When worn out, are eliminated by phagocytes in the spleen or liver
CONTROL OF ERYTHROCYTE PRODUCTION
Erythropoietin: hormone that controls the rate of erythrocyte production
Kidneys produce most erythropoietin as a response to reduced oxygen levels in the blood
Homeostasis is maintained by negative feedback from blood oxygen levels
What happens if there is renal failure or is undergoing dialysis?
Reduced erythropoietin production—> decreased oxygen carrying capacity of the blood (pale symptoms, connected to anemia)
HEMOSTASIS
Stoppage of blood flow result of a break in a blood vessel
Hemostasis involves three phases
Platelet plug formation
Collagen fibers are exposed by a break in a blood vessel
Platelets become “sticky” and cling to fibers
Anchored platelets release chemicals to attract more platelets
Platelets pile up to form a platelet plug
Stops the bleeding
Vascular spasms
Anchored platelets release serotonin
Serotonin causes blood vessel muscles to spasm
Spasms narrow the blood vessel, decreasing blood loss
Coagulation
Injured tissues release thromboplastin
PF3 (a phospholipid) interacts with thromboplastin, blood protein. clotting factors, and calcium ions to trigger a clotting cascade
Prothrombin activator converts prothrombin to thrombin (an enzyme)
Thrombin joins fibrinogen proteins into hair-like fibrin
Fibrin forms a meshwork
Meshwork: basis for a clot
BLOOD CLOTTING
Blood usually clots within 3 to 6 minutes
clot remains as endothelium regenerates
clot is broken down after tissue repair
FIBRIN CLOT
UNDESIRABLE CLOTTING
Thrombus: a clot in an unbroken blood vessel
Can be deadly in areas like the heart
Embolus: A thrombus that breaks away and floats freely in the bloodstream
Clot can be dislodged and become an embolus
Can later clog vessels in critical areas such as the brain
Can be deadly in areas like the heart
Fatty foods
Effect of thrombi: blood flow is decreased; heart rate is increased
BLEEDING DISORDERS
Thrombocytopenia: Platelet deficiency
Even normal movements can cause bleeding from small blood vessels that require platelets for clotting
Hemophilia: Hereditary bleeding disorder
Normal clotting factors are missing
3rd phase is abnormal
BLOOD GROUPS AND TRANSFUSIONS
Large losses of blood have serious consequences
Weakness: Caused by a loss of blood of 15-30%
Shock: caused by a loss of over 30% of blood (fatal)
sepsis can lead to shock
Toxic shock syndrome
Hypovolemic shock: severe blood or other fluid loss makes the heart unable to pump enough blood to the body.
Transfusions: the only way to replace blood quickly
Transfused blood must be of the same blood group
Why do they have to be the same Blood group?
causes hypersensitivity
HUMAN BLOOD GROUPS
Blood contains genetically determined proteins
Antigen: a foreign protein that may be attacked by the immune system
Blood is “typed” by using antibodies that will cause blood with certain proteins to clump
agglutination: when proteins start to clump
There are over 30 common red blood cell antigens
ABO and Rh blood group antigens: cause the most vigorous transfusion reactions
ABO BLOOD GROUPS
Based on the presence or absence of 2 antigens
Type A: presence of A antigens
Type B: presence of B antigens
Type O: lack of these antigens
Type AB: presence of A & B antigens
Rh BLOOD GROUPS
Named because of the presence or absence of one of eight Rh antigens (agglutinogen D)
Most Americans are Rh+
Problems can occur in mixing Rh+ blood into a body with Rh– blood
Rh DANGERS DURING PREGNANCY
Danger is only when the mother is Rh– and the father is Rh+, and the child inherits the Rh+ factor
Mismatch of an Rh- mother, carrying an Rh+ baby→ can cause problems for the unborn child
The first pregnancy usually proceeds without problems
The immune system is sensitized after the first pregnancy
Hemolytic Disease of the Newborn: In a second pregnancy, the mother’s immune system produces antibodies to attack the Rh+ blood
UNDESIRABLE CLOTTING
Blood samples are mixed with anti-A and anti-B serum
Coagulation or no coagulation: leads to determining blood type
Typing for ABO and Rh factors is done in the same manner
Cross matching: testing for agglutination of donor RBCs by the recipient’s serum, and vice versa
BLOOD GROUPS AND TRANSFUSIONS
Sites of blood cell formation
The fetal liver and spleen are early sites of blood cell formation
Bone marrow takes over hematopoiesis by the seventh month
Fetal hemoglobin differs from hemoglobin produced after birth
Jaundice: hemolisis