Test 1: Blood, Heart, & Cardiovascular System Flashcards
Blood is made up of the following
- Plasma: Water, Solutes (electrolytes, vitamins, etc), proteins, antigens etc.
- Formed Elements: RBC, WBC, and Platlets
Formed elements in blood
- Erythrocytes (RBC)
- Platelets
- Leukocytes (WBC)- 5 total/ 2 categories:
granulocytes (with granules)
- neutrophils
- eosinophils
- basophils
agranulocytes (without granules)
- lymphocytes
- monocytes
Name these formed elements in blood
A.Monocyte
B.Platelets
C.Small Lymphocyte
D.Neutrophil
E.Large Lymphocyte
F.Basophil
G.Small Lymphocyte
H.Neutrophil
I.Eosinophil
J.Erthyrocyte
K.Young Neutrophil
L.Monocyte
M.Neutrophil
Plasma Components
- Water
- Proteins
- Nutrients
- Electrolytes
- Nitrogenous Waste
- Hormones
- Gases
Plasma Proteins & Function
Formed by the liver (except globulins)
- Albumins: smallest and most abundant
* Contribute to and osmolarity; influence blood pressure, flow, and fluid balance viscosity - Globulins (Antibodies)
- Provide immune system functions
- Alpha, beta, and gamma globulins
- Fibrinogen
* Precursor of fibrin threads that help form blood clots - Haptogloblulin: transports hemoglobin released by dead erthytocytes
- Ceuloplasmin: transports copper
- Prothombin: promotes blood clotting
- Transferrin: transports iron
Plasma Nitrogenous Compounds
–Free amino acids from dietary protein or tissue breakdown
–Nitrogenous wastes (urea)
- Toxic end products of catabolism
- Normally removed by the kidneys
Plasma Nutrients
- Glucose
- Vitamins
- Fats
- Cholesterol
- Phospholipids,
- Minerals
Plasma Electrolytes
- Na+ : makes up 90% of plasma cations
- K+
- Cl-
- Ca2+
Plasma Gases
-Dissolved O2, CO2, and Nitrogen
Erythocyte: Structure & Function
- *Structure:**
- Disc shaped cell with thick rim
–Lose nearly all organelles during development
•Lack mitochondria
- Anaerobic fermentation to produce ATP
•Lack of nucleus and DNA
- No protein synthesis or mitosis
- Blood type determined by surface glycoproteins and glycolipids
•Stretch and bend as squeezed through small capillaries
Cytoskeletal proteins (spectrin and actin) give membrane durability and resilience
Function:
1.Gas Transport
–Carry oxygen from lungs to cell tissues
–Pick up CO_2 from tissues and bring to lungs
Blood Type & How They Are Determined
Antigen (Flags)
Types:
A+
A-
B+
B-
AB+
AB-
O+
O-
Important structural components in Erythrocytes that allow for its function
Important role in gas transport and pH balance
–Increased surface area/volume ratio
- Due to loss of organelles during maturation
- Increases diffusion rate of substances
–33% of cytoplasm is hemoglobin (Hb)
- 280 million hemoglobin molecules on one RBC
- O2 delivery to tissue and CO2 transport to lungs
- Carbonic anhydrase (CAH) in cytoplasm
–Produces carbonic acid from CO_2 and water
Leukocyte: Structure & Function
•Least abundant formed element
»5,000 to 10,000 WBCs/μL
- Protect against infectious microorganisms and other pathogens
- Conspicuous nucleus
- Spend only a few hours in the bloodstream before migrating to connective tissue
- Retain their organelles for protein synthesis
- Granule Presence in some
- All WBCs have lysosomes called nonspecific (azurophilic) granules
- Granulocytes (some WBCs) have specific granules that contain enzymes and other chemicals employed in defense against pathogens
Neutrophil: Stucture & Function
Structure:
–Neutrophils (60% to 70%): polymorphonuclear leukocytes
•Barely visible granules in cytoplasm; three- to five-lobed nucleus
Function:
•aggressively antibacterial
–Neutrophilia—rise in number of neutrophils in response to bacterial infection
Purpose of granulocytes
Contain enzymes and other chemicals employed in defense against pathogens
Eosinophils
Structure:
- Granulocyte
- –(2% to 4%)
•Large rosy-orange granules; bilobed nucleus
Function
•increased numbers in parasitic infections, collagen diseases, allergies, diseases of spleen and CNS
-Phagocytosis of antigen–antibody complexes,
allergens, and inflammatory chemicals
–Release enzymes to destroy large parasites
Basophils: Structure & Function
Structure:
- Granulocyte
- (less than 1%)
•Large, abundant, violet granules (obscure a large S-shaped nucleus)
Function:
- Increased numbers in chickenpox, sinusitis, diabetes
- Secrete histamine (vasodilator): speeds flow of blood to an injured area
- Secrete heparin (anticoagulant): promotes the mobility of other WBCs in the area
Lymphoctes: Structure & Function
Structure:
–(25% to 33%)
•Variable amounts of bluish cytoplasm (scanty to abundant); ovoid/round, uniform dark violet nucleus
Function:
•Lymphocytes—increased numbers in diverse infections and immune responses
–Destroy cells (cancer, foreign, and virally infected cells)
–“Present” antigens to activate other immune cells
–Coordinate actions of other immune cells
Secrete antibodies and provide immune memory
Monocytes: Structure & Function
Structure:
–Monocytes (3% to 8%)
•Usually largest WBC; ovoid, kidney-, or horseshoe-shaped nucleus
Function:
•increased numbers in viral infections and inflammation
–Leave bloodstream and transform into macrophages
- Phagocytize pathogens and debris
- “Present” antigens to activate other immune cells—antigen-presenting cells (APCs)
Platelet: Structure & Function
Structure:
-
•Platelets—small fragments of megakaryocyte cells
–2 to 4 μm diameter; contain “granules”
–Platelet contains a complex internal structure and an open canalicular system
–Amoeboid movement and phagocytosis
•Normal platelet count—130,000 to 400,000 platelets/μL
Function:
–Secrete vasoconstrictors that help reduce blood loss
–Stick together to form platelet plugs to seal small breaks
–Secrete procoagulants or clotting factors to promote clotting
–Initiate formation of clot-dissolving enzyme
–Chemically attract neutrophils and monocytes to sites of inflammation
–Phagocytize and destroy bacteria
–Secrete growth factors that stimulate mitosis to repair blood vessels
Blood Properties
- Viscosity
- Osmolarity
Blood Viscosity
•Viscosity—resistance of a fluid to flow, resulting from the cohesion of its particles
–Whole blood 4.5 to 5.5 times as viscous as water
–Plasma is 2.0 times as viscous as water
•Important in circulatory function
ie: results from the cohesion of its particles. It is the thickness or stickiness of a fluid.
*An RBC or protein deficiency reduces viscosity. and causes the blood to flow too easily. Where as an excess can cause the blood to move in a sluggish way.Either condition puts a strain on the heart and can lead to serious cariovasular problems.
Blood Osmolarity
•Osmolarity of blood—the total molarity of those dissolved particles that cannot pass through the blood vessel wall
–If too high, blood absorbs too much water, increasing the blood pressure
–If too low, too much water stays in tissue, blood pressure drops, and edema occurs
–Optimum osmolarity is achieved by the body’s regulation of sodium ions, proteins, and red blood cells
Hematocrit
Also known as packed cell volume
•centrifuge blood to separate components
–Erythrocytes are heaviest and settle first
•37% to 52% total volume
–White blood cells and platelets
- 1% total volume
- Buffy coat
–Plasma
- The remainder of volume
- 47% to 63%
- Complex mixture of water, proteins, nutrients, electrolytes, nitrogenous wastes, hormones, and gases
Blood Fractionation
Seperation of blood components based on relative densities.
Centrifugation is a method that allows for fractionation.
Erythopoesis
- Erythroposis = erythrocyte production
- 1 million RBCs are produced per second
- Average lifespan of about 120 days
- Development takes 3 to 5 days
Steps:
- Hematopoietic stem cell (HSC) becomes an erythcte colony forming unit (ECFU) - has receptors for erythropoetin (EPI), a hormone secreted by the kidneys
- EPO stimulates the ECFU to transofrm into an erythroblast
- Erythroblasts multiply , build up large cell population.
- Once complete, nucleus shrivels and is discharged from cell- the cell is now called a reticulocyte.
- Reticulocyte leave the bone marrow and enter the citculating blood. Within a day or two, the last of the polyribosomes disintegrate and disappear, and the cell is a matrue erythrocyte.
*About 0.5-1% of circulating RBC are reticulocytes but the percentage may rise under certain circumstances. Blood loss would stimulate erythropoesis.
Leukopoesis
Leukopoesis= production of WBC
Begins with the same HSC as erythropoesis
Some HSC differentiate into distinct types of CFU and then go on to form the following cell lines
- Myeloblasts: ultimately differentiate into 3 types of granulocytes (neutrophils, eosinophils, and basophils)
- Monoblasts- which look identical to myeloblast but lead to monocytes
- Lymphoblasts: which proucte all lymphocytes
•Red bone marrow stores and releases granulocytes and monocytes
CFUS have receptors for colony stimulating factors- mature lymphocytes and macrophages secrete several types of CSFs in response to infections and other immune challenges. Each CSF stimulates a different WBC to develop in response to specific needs. Thus a bacterial infection may trigger the production of neutrophils whereas an allergy stimulates oesinophil prouction, each procress working through its own CSF!
Leukocyte Life Cycle
•Circulating WBCs do not stay in bloodstream
–Granulocytes leave in 8 hours and live 5 days longer
–Monocytes leave in 20 hours, transform into macrophages, and live for several years
–Lymphocytes provide long-term immunity (decades), being continuously recycled from blood to tissue fluid to lymph and back to the blood
Hemoglobin
Structure:
Makes up 33% of RBC
consists of fout protein chains called globins, two are alpha and two are beta
Each chain is conjugatred with a nonprotein moeity called the heme group.
Heme group: bind oxygen to an iron atom.
Function:
Gives RBC its red color
Involved in oxygen transsports
Also aids in carrying away CO2 and buffering blood pH
Heparin
- An anticoagulant released by Basophils
- promotes the mobility of other WBCs in the area
Histamine
- A vasodilator
- Example: released by Basophilsas a way to speed flow of blood to an injured area
Growth Factors
-Platlets secrete growth factors that stimulate mitosis to repair blood vessels
Serotonin
- Vasoconstrictor
- Example: platlets will release during hemostatis during vasccular spasm stage (prompt constriction of a broken vessel- most immediate protection against blood loss)
Thromboxane A2
- An eicosanoid, promotes platelet aggregation, degranulation, and vasoconstriction
- Example: used during platelet plug formation
Erthrocyte Disorders
- Any imbalance between the rates of erythopoesis and RBC destruction may produce an excess or deficiency of red cells.
- RBC Excess: polycythemia
- RBC Deficiency: Anemia
Polycythemia
•an excess of RBCs
–Primary polycythemia (polycythemia vera)
•Cancer of erythropoietic cell line in red bone marrow
–RBC count as high as 11 million RBCs/μL; hematocrit 80%
–Secondary polycythemia
•From dehydration, emphysema, high altitude, or physical conditioning
–RBC count up to 8 million RBCs/μL
•Dangers of polycythemia
–Increased blood volume, pressure, viscosity
Can lead to embolism, stroke, or heart failure
Anemia Types
•Causes of anemia fall into three categories
1.Inadequate erythropoiesis or hemoglobin synthesis
- Kidney failure and insufficient erythropoietin
- Iron-deficiency anemia
- Pernicious anemia—autoimmune attack of stomach tissue leads to inadequate vitamin B_12 absorption
- Hypoplastic anemia—slowing of erythropoiesis
- Aplastic anemia—complete cessation of erythropoiesis
- Hemorrhagic anemias from bleeding
- Hemolytic anemias from RBC destruction
Anemia Consequences
–Tissue hypoxia and necrosis
- Patient is lethargic
- Shortness of breath upon exertion
- Life-threatening necrosis of brain, heart, or kidney
–Blood osmolarity is reduced, producing tissue edema
–Blood viscosity is low
•Heart races and pressure drops
Cardiac failure may ensue
Sickle Cell Disease
- Hereditary defects that occur mostly among people of African descent
- Caused by recessive allele that modifies structure of Hb (makes HbS)
–Differs only on the sixth amino acid of the beta chain
–HbS does not bind oxygen well
–RBCs become rigid, sticky, pointed at ends
–Clump together and block small blood vessels
–Can lead to kidney or heart failure, stroke, joint pain, or paralysis
–Heterozygotes (only one sickle cell allele) are resistant to malaria
Leukocyte Disorders: Types
Normal WBC Count: 5,000-10,000 WBC/ µL
- Lekopenia= a count below this
- Leukocytosis= a count above this
- **Leukemia: cancer of hematopoteic tissues that usually produces an extradoinarly high level of leukoctyes and their precurots.
Leukopenia
•low WBC count: below 5,000 WBCs/μL
–Causes: radiation, poisons, infectious disease
–Effects: elevated risk of infection
Leukocytosis
—high WBC count: above 10,000 WBCs/μL
–Causes: infection, allergy, disease
–Differential WBC count: identifies what percentage of the total WBC count consist of each type of leukocyte
Leukemia
•Leukemia—cancer of hemopoietic tissue usually producing a very high number of circulating leukocytes
–Myeloid leukemia: uncontrolled granulocyte production
–Lymphoid leukemia: uncontrolled lymphocyte or monocyte production
–Acute leukemia: appears suddenly, progresses rapidly, death within months
–Chronic leukemia: undetected for months, survival time 3 years
–Effects: normal cell percentages disrupted; impaired clotting; opportunistic infections
Microscope
Platelet/ Clotting Disorders: Types
•Deficiency of any clotting factor can shut down the coagulation cascade
- Hemophilia: family of hereditary diseases characterized by deficiencies of one factor or another
- Physical exertion causes bleeding and excruciating pain
- Hematomas—masses of clotted blood in the tissues
- Thrombosis—abnormal clotting in unbroken vessel
- Infarction (tissue death) may occur if clot blocks blood supply to an organ (MI or stroke)
Clotting Disorders: Physical Exertion
•Physical exertion causes bleeding and excruciating pain
–Transfusion of plasma or purified clotting factors
–Factor VIII produced by transgenic bacteria
Clotting Disorders: Thrombosis
•Thrombosis—abnormal clotting in unbroken vessel
–Thrombus: clot
•Most likely to occur in leg veins of inactive people
–Pulmonary embolism: clot may break free, travel from veins to lungs
•Embolus—anything that can travel in the blood and block blood vessels
Clotting Disorders: Infarction
•Infarction (tissue death) may occur if clot blocks blood supply to an organ (MI or stroke)
–650,000 Americans die annually of thromboembolism (traveling blood clots)
Clotting Disorders: Hemophilia
- Hemophilia—family of hereditary diseases characterized by deficiencies of one factor or another
- Sex-linked recessive (on X chromosome)
–Hemophilia A missing factor VIII (83% of cases)
–Hemophilia B missing factor IX (15% of cases)
Hemophilia C missing factor XI (autosomal)
Clotting Disorders: Hematomas
masses of clotted blood in the tissues
Platelet Production
•Thrombopoiesis
–Stem cells (that develop receptors for thrombopoietin) become megakaryoblasts
•Megakaryoblasts
–Repeatedly replicate DNA without dividing
–Form gigantic cells called megakaryocytes with a multilobed nucleus
- 100 mm in diameter, remains in bone marrow
- Megakaryocytes—live in bone marrow adjacent to blood sinusoids
–Long tendrils of cytoplasm (proplatelets) protrude into the blood sinusoids: blood flow splits off fragments called platelets
•Platelets circulate freely for 5-6 days
–40% are stored in spleen
Platelet Structure
Structure:
•Platelets—small fragments of megakaryocyte cells
–2 to 4 μm diameter; contain “granules”
–Platelet contains a complex internal structure and an open canalicular system
–Amoeboid movement and phagocytosis
•Normal platelet count—130,000 to 400,000 platelets/μL
Platelet Function
•Platelet functions
–Secrete vasoconstrictors that help reduce blood loss
–Stick together to form platelet plugs to seal small breaks
–Secrete procoagulants or clotting factors to promote clotting
–Initiate formation of clot-dissolving enzyme
–Chemically attract neutrophils and monocytes to sites of inflammation
–Phagocytize and destroy bacteria
–Secrete growth factors that stimulate mitosis to repair blood vessels
Circulatory System
Heart, Blood Vessels, and Blood
Cardiovascular System
Heart & Blood Vessels
Systemic Circuit
- Left side of the heart
- Fully oxygenated blood arrives from the lungs via pulmonary veins
- Blood sent to all organs of the of the body via the aorta
- Thicker Walls to provide more pressure to pump blood throughout the body
Pulmonary Circuit
- Right side of the heart
- Oxygen-poor blood arrives from the inferior & superior vena cava venae cavae
- Blood sent to the lungs via the pulmonary trunk
How can you distinguish between the systemic and pulmonary circuits ?
Pulmonary Circuit
- Pulmonary circulation carries deoxygenated blood from the right ventricle of the heart to the lungs through the pulmonary artery
- Carries oxygenated blood from the lungs to the left atrium of the heart by the pulmonary vein
- Composed of pulmonary artery and pulmonary vein
- Carries blood to the lungs
- Helps to release carbon dioxide from the blood while dissoliving oxygen in the blood
Systemic Circuit
- Systemic Circulation carries oxygenated blood from the left ventricle of the heart to the rest of the body by the aorta
- Carries deoxgenated blood from the body to the right atrium of the heart by the superior and inferior vena cava
- Composed of the inferior and superior vena cava, aorta, and other small blood vessles
- Carries blood throughout the body (including heart)
- Helps to provide nutrients and oxygen to the metabolizing cells in the body
How does the heart supply itself with the oxygen and remove CO2 ?
- Via Coronary Circulation
- Not done through the heart chambers but instead through diffusion of substances through the myocardium
- Myocardium has its own supply of arteries and cappilaries that deliver blood to every muscle cell
- CO2 is removed / drained from the coronary sinus veins
Name these parts
A.Great Cardiac Vein
B.Circumflex branch of Left Cornary Artery (LCA)
C.Coronary Sinus
D.Left marginal branch of LCA
E.Right Coronary Artery (RCA)
F.Right marginal branch of RCA
G.Posterior interventricular branch of RCA
H.Posterior interventricular vein
I.Posterior View
Name these parts
A.RCA
B.Small Cardiac Vein
C.Right marginal branch of RCA
D.LCA
E.Left auricle
F.Circumflex branch of LCA
G.Great Cardiac Vein
H.Anterior interventricular branch of LCA
I.Anterior View
Arterial Supply (anterior)
•Left coronary artery (LCA) branches off the ascending aorta
–Anterior interventricular branch
•Supplies blood to both ventricles and anterior two-thirds of the interventricular septum
–Circumflex branch
- Passes around left side of heart in coronary sulcus
- Gives off left marginal branch and then ends on the posterior side of the heart
- Supplies left atrium and posterior wall of left ventricle
Arterial Supply (Posterior)
•Right coronary artery (RCA) branches off the ascending aorta
–Supplies right atrium and sinoatrial node (pacemaker)
–Right marginal branch
•Supplies lateral aspect of right atrium and ventricle
–Posterior interventricular branch
•Supplies posterior walls of ventricles
Arterial Supply Flow
Flow through coronary arteries is greatest when heart relaxes
Contraction of the myocardium compresses the coronary arteries and obstructs blood flow
Opening of the aortic valve flap during ventricular systole covers the openings to the coronary arteries blocking blood flow into them
During ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries
Myocardial Infarction
A fatty deposit or blood clot in a coronoary artery can cause MI
How can you distinguish between the anterior and posterior heart views
Anterior View:
- Apex is to the right
- Superior Vena Cava is full
Posterior View
- Apex to the left
- Inferior Vena Cava is full
What are the specific characterisitcs of the heart: Position, Size, and Shape ?
Position, Size, and Shape of Heart
- Lie within a thick partition called the mediastinum medial (between) the lungs
- Apex is obliqued plane
- Located in thoracic region
- Located above diaphram
- Size of a fist at any age
- 4 chambers
- 4 valves
- Base- wide superior portion of the heart
What specific disorders are associated with abnormalities of heart structure ?
A structural issue that is congential = present at birth or developed over time from wear and tear or as a result of another disease
- Size= enlarged heart
* Example: Cardiomyopathy - enlarged chambers & less musculatre OR Myocarditis- inflammed muscles, larger chambers. - Valvular Insuffiency: any failure of a valve to prevent reflux- backward floor of blood
i. Valvular Stenuses: narrowing of valve-> restricts forward flow of blood
cusps are stiffened and opening is constricted by scar tissue
- Result of rheumatic fever, autoimmune attack on the mitral and aortic valves
- Heart overworks and may become enlarged
- Heart murmur—abnormal heart sound produced by regurgitation of blood through incompetent valve
ii.Valvular Incompetence
- failure of valve to close completely, flaps back
- blood regurgitates or leaks backwards
- Example 1: Mitroal Valve: insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction
- Hereditary in 1 out of 40 people
- May cause chest pain and shortness of breath
- Example 2: Aoartic Stenosis- aortic valve doesn’t completely open.
- Pericarditis: inflammation of the pericardium ?
- Holes in the heart (Septal Defects): opening between the atria or the ventricles
5
Types of Anemia
Inadqueate Erythropoesis
- Iron Deficiency Anemia
- Other Nutritional Anemia ie. Folic Acid
- Anemia due to renal insufficiency
- Pernicious Anemia: Vitamin B12
- Hypoplastic and aplastic anemia
- Anemia of old age
Blood Loss Anemia
- Hereditary clotting deficneicnes
- Non hereditary causes
RBC Destruction
- Drug reactions
- Poisoning
- Parasetic infection
- Hereditary hemoglobin defects
- Blood Type Incapabilities
What are the specific characterisitcs of the heart: Pericardium?
- Surrounded by Pericardium, a double-walled sac
- Pericardium
- Outer (tough fibrous sac) = fibrous pericardium
- Inner (thin membrane) = serous pericardium
- parietal layer= deeper layer
- visceral= most superficial layer.. forms the outermost layer of heart (the epicardium)
- Pericardial Cavity= space between the double layer of the serous pericardium
Function:
- reduces friction
- isolates the heart from other thoracic organs and anchors it within the thorax
- allows for heart expansion but not too much expansion
Pericarditis
- Inflammation of the pericardium
- Membranes are roughened and produce a painful friction rub with each heartbeat
What are the specific characterisitcs of the heart: Heart Wall ?
Three Layers:
- Epicardium =visceral layer of the serous pericardium
- Myocardium= lays btw. epicardium and endocardium. This is the thickest layer and performs the work of th heart. Thickness is proportional to the wrokload of the individual chambers.
- Endocardium= lines the interior of the heart chamber
What are the specific characterisitcs of the heart: The Chambers ?
Internal
- Four chambers
- Superior: right/ left atria- mostly on posterior side
- Inferior: left/ right ventricles-
- Interatrial Septum = seperate the atrium
- Interventricular Septum= seperate the ventricles
- Right Ventricle only pumps blood to the lungs and the left atrium so its wall is moderately muscular
- Left Ventricle is 2-4 X thick because it bears the greatest workload of all four chambers, pumping blood throughout the body.
- Left ventricle- circcular in cross section
- Right ventricle- c-shaped in cross section
Surface
- 3 sulci divide the boundaries of the four chambers. They harbor the largrest of the coronary blood vesseles
- Coronary Sulcus: seperate atria from ventricles
- Anterior interventrical sulci: seperate ventricles
- Posterior interventrical sulci
What are the specific characterisitcs of the heart: The Valves ?
- One way valves between each atrium and ventricle AND between ventricle and exit vessel (great artery)
- Cusps of valve open and close by changes in blood pressure that occur as the heart chambers contract and relax
- AV Valve: Anterior Ventricular Valve
- Right= tricuspid.. three cusps
- Left (Mitral)= bicuspid.. two cusps
- Semilunar Valve (pulmonary and aortic valve)
- Pulmonary Valve = right ventricle> pulmonary trunk
- Aoartic valve = left ventricle > aorta
Blood flow through the chambers
- Blood enters right atrium from the superior and inferior vena cava
- Blood in the right atrium flows through the right AV valve intro the right ventricle
- Contraction of the right ventricle forces the pulmonary valve to open
- Blood flows through the pulmonary valve and intro the pulmonary trunk
- Blood is distributed by the right andleft pulmonary arteries to the lunges, where it unloads CO2 and loads O2
- Blood returns to the lungs via the pulmonary veins to the left atrium
- Blood in left atrium flows through left AV valve into left ventricle
- Contraction of left ventricle (simulatanous with step 3) forces aortic valve to open
- Blood flows through aortic valve into ascending aorta
- blood in the aorta is distributed to every organ in the body, where it unloads O2 and loads C02
- Blood returns to the right atrium via the vena cavae
Do arteries always carry oxygenated blood and veins oxygen poor blood?
- Veins bring blood to the heart AND arteries carry blood away from the heart
- While most veins carry deoxygenated blood and arteries carry oxygenated blood there are expections
- Left/Right Pulmonary Veins bring oxygenated blood to the left atrium
- Left/ Right Pulmonary Arteries carry doxgenated blood away from right ventricle
Electrical activity during blood flow through the chambers
•Coordinates the heartbeat
- SA Node Fires- depolirization
- Modified cardiomyocyte
- Internal Pacemakers
(automaticity- doesn’t need a neighbor )
- Excitation spreads through atrial myocardium - neighboring cells AND contraction occurs in the atrium
- AV node fires (connection between the atrium and ventricles)- creates a delay between the atria and ventricle contractions.
* Coordinated flow - Excitation spreads down AV bundle (bundle of His)
- Subendocardial conducting network distributes excitation through ventricular myocardium- purkinje fibers
Blood flow/ electrical activity and heart sounds?
- First heart sound (S_1), louder and longer “lubb,” occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall
- Second heart sound (S_2), softer and sharper “dupp,” occurs with closure of semilunar/ aaortic valves, turbulence in the bloodstream, and movements of the heart wall
- S_3—rarely heard in people over 30
Think of different situations when a family friend comes to you for an advice regarding a specific symptom related to the heart/blood disorders and what tests you could recommend them and why?
- Vitals
- EKG
- Basic Metabolic Panel (BMP): detect levels of glucose, chloride, sodium, potassium, CO2, creatinine, blood urea nitrogen, etc.
- Glucose = signs of diabetes
- Chloride= acid- base balance
- Sodium= nerve conduction/ muscle contraction
- Potassium = nerve conduction/ muscle contraction
- CO2 = respitory difficulties
- Creatinine = muscle metabolism, preeclampsia or eclampsia
- Blood Urea Nitrogen= kidney disease
- Complete Blood Count- process of diagonsing an llness frequently requires examination of CBC. A sample of blood is drawn from the patient and sent to lab for testing. Report gives wide range of information about the blood- comparing patients blood values to a normal range. Any range outside the norm can indicate a potential problem.
Tests within a CBC:
- WBC Count
- WBC Differential = % of WBC types
- RBC Count
- Hemoglobin amt.
- Platlet count
- Baisc
Cardiovascular vs Circulartory System
Cardiovascular = heart & blood vessels
Circulartory = heart, blood vessels, & blood
Lub-Dub Sounds
Lub Sound= Tricuspid + Bicuspid Valve closure
Dub Sound = Pulmonary Semilunar + Aoartic Valve closure
What are the characterisitcs of the cardiac muscle that allow it to function properly ?
Cardiomyocytes = heart muscle
- Single or multiple nucluei
- Nucleus surrounded by glycogen storage
- Cardiomyocytes are joined together by intercolated discs
- Cardiac muscles lack satellite cells that divide and replace dead muscle fibers- repair of damaged cardiac muscle is almost done entirely by fibrosis (scarring)- limited capacity for mitosis and regeneration.
- Metabolism & Mitochondria:
- Huge mitochondria (bigger than found in skeletal muscle cells)
- Leans on aerobic respiration- doesn’t fatigue easily
- Very adaptable to organic fuels used: fatty acids, glucose, ketones, amino acids, etc.
2.Energy Storage:
- Rich in myoglobin- short term oxygen
- Rich in glyocogen- long term energy storage
3.Communication- entire myocardium behaves almost like a single cell- creating a unified action essential for heart pumping
- Tightly bound by intercalated discs: interdigitating folds and mechanical junctions (desosomes and facsia adherens) keep the cardiomyocytes held togther
- Electrical gap junctions form channels to allow for electrical conduction to pass easily from one cardiomyocyte to a nieghboring muscle cell.
Symphathetic Nervous System AND Heart Beat: Signaling Molecules & Function
- Epinephrine and epinephrine bind to Beta Adrenogenic Receptors in the heart and activate the cAMP
- cAMP activates an enzyme that opens Calcium channels in the plasma membrane, admitting calcium from the ECF into the SA Node and cardiomyocytes .
–> This speeds up depolirization of the SA node and speeds up signal confuction through the AV node, thereby quickening the contractions of the ventricular myocardium and heartbeat!
3.cAMP will also facilitate reuptake of Calcium in the S.R of the cardiomyocytes which shortens ventrical systole and QT interval allowing for the ventricles to relax and refill sooner than they do at rest
Cariac Output
The amount ejected by each ventircle in 1 minute is called the cardiac output (CO).
CO = HR x SV
HR: Heart Rate (Beats per minute)
SV: Stroke Volume (mL/beat)
Cardiac Output & Exercise
Cardiac output varies with the body’s state of activity. Example: Vigorous exercise increase CO
Routine Exercise programming will cause hypertrophy of ventricles which will increase its stroke volume. An athlete heartrate can beat more slowly yet still have higher CO because their stroke volume is high.
Some world class athletes have resting heart rates at 30-40 BPM but because of higher stroke volume, their resting cardiac output is the same as an untrained person. Such athletes have greater cardiac reserve since they can tolerate more exertion than a sedentary person.
Cardiac Reserve
Difference between maxium and resting cardiac output is called cardiac reserve
People with severe heart disease may have little or no cardiac reserve and little tolerance to physical exertion.
Positive vs Negative Chronotropic Agents
Positive Chronotropic Factors: outside of the heart that raise the heart rate.
Negative Chronotropic Factors: outside of the heart that lower the heart rate.
cAMP Function in Sympathetic Nervous System
Increases heart rate by accelerating contraction and relaxation of the heart
Epinephrine/ Norepinephrine Function in ANS
Sympathetic ; Speed up the heart rate by activating cAMP
Cardiac Output/ Reserve and Heart Beat
Increasing heart beat frequency will reduce cardiac output and reserve because the heart doesnt have enough time to rest and refill with blood
Parasympathetic Nervous System AND Heart Beat: Signaling Molecules & Function
- Vagus Nerve innervates SA & AV Node and release Acetylcholine (ACh)
- ACh bind to muscle receptor and open potassium gates which causes outflow of potassium –> leading to hyperpolerization of the muscle cell
- SA Node fires less frequently as a result and heart rate slows down. AV Node also gets signaled by ACH and hyperpolerized which delays excitation at the ventricles
ACh vs NE/ Epi Pathway & Effect
ACH has a direct line to act on membrane ion channels where as NE/ Epi need to signal cAMP cascade for activity. Thereforefore, vagus nerves act quicker on the heart than the sympathetic nervous system
Receptor Types within cardiovascular system
Signaling recieved by the medulla
Types:
- Propireceptors: within muscle and joints provide information on changes in physical activity.
- Baroreceptors: pressure receptors in the aorta and internal caratid arteries.
- When > heart rate rises> cardiac output increases> blood pressure increases. Baroreceptors can communicate with medulla to then trigger the vagal output to lower heart rate. It can also issue a sympathetic output to increase heart rate to bring CO and blood pressure back to normal.
- Chemoreceptors: sensitive to blood pH, CO2, and O2.
- If circulation to tissues is too slow to remove CO2> CO2 accumulates to the blood (hypercapnia) and pH can become more acidic (acidosis)> chemoreceptors sense> signal to increase heart rate and improve perfusion of tissues to restore homeostatis
- Oxygen deficiency (hypoxemia) may lead to triggering slow down heart rate so heart doesn’t compete with brain for limited oxygen supply.
Signaling molecules that affect heart rate
- Potassium (in Hyperkalemia and Hypokalemia):
- Hyperkalemia: potassium excess. too much K inters the cell and makes it too positive, making it difficult to hyperpolerize. Heart Rate will slow down
- Hypokalemia: potassium deficiency. too much K leaves the cell and makes it too negative and hard to excite/ stimulate
- Calcium (Hypercalemia and Hypocalcemia)
- Hypercalcemia: causes a slow heartbeat
- Hypocalcemia: elevates heart rate
Coronary Artery Disease
Accumulation of lipid deposits/ placque that degrade the aetrial wall and obstruct the lumen.
- aeterial lining becomes damaged
- monocytes adhere, penetrate the lining and become macrophages.
- Macrophages and smooth muscles absorb chlolestorol and fat from the blood which can form into artheromas (placques)
- Placques can grow and form into lipid, fiber, and other cells
Symptoms:
- Angina Pectoris
- Placque can lodge free and clog smaller artery elsewhere
- Spasms can cut off blood supply to myocardium (angina can form as a result)
- Harderning of placque can lead to aterioscelrosis -> blood pressure increase, stroke, kidney failure
Worst form of coronary heart disease?
Myocardial Infarction
Name these processes
A= Atria Contract
B= Ventricles Contract
P Wave = Atrial Depolirization
QRS Complex = Ventricular Depolarization
T Wave =Ventricular Repolirization
QT Interval = Duration of ventricular depolarization; shorter during exercise
QRS Interval = Atrial repolarization and diastole; repolarization concealed by QRS wave
PQ segment = Signal conduction from SA node to AV node, atrial sustole begins
ST Segment: Ventricular Sytole and ejection of blood
SA: Electrical Signaling in heart & ions/ channels involved
Firing of AV Node leads to Atrial Contraction
- When pacemaker potential reaches -40mV, voltage gated calcium channels open and Calcium flows in causing depolarization
- At 0 mV Potassium channels open and K leaves the cell, causing repolarization
When repolarization is complete, the potassium channels close and the pacmaker potential starts over to produce next heartbeat.
AV Node: electrical signaling in the heart & ions/ channels involved
AV node firing is responsible for ventricular contraction. Signaling is slower due to thinner walls and communication between cardiomyocytes> causing a delay > allowing for the ventricles to refill
- Stimulus causes SA channels to open
- NA influx depolarizes cell and leads to more NA channels to open (positive feedback cycle) , creating rapidly rising membrane voltage.
- Na channels close when cell reaches +30 mV
- Calcium channels open and slow inflow prolongs depolarization
- Calcium channels close and calcium is transported out of cell. Potassium channels open and potassium leaves the cell. Shift leads to return of resting membrane potential –> muscle tension is released shortly after.
Blood Formed Element Developments
1.RBC
A.HSC
B. Several Intermediate Progenitors and will deferentiating by developing surface receptors that attract a stimulating factor. **With RBC, EPO triggers development
C. Reticulocytes Form > RBC.. nucleus is lost in process
- WBC
A. HSC forms into CSF (commitment to path)
B.CSF > kept at a constant low number but production can increased greatly and quickly in response to foreign invaders
C.
- Platelet
A.Stimulated by thrombopoetin TPO
B. Leads to formation of megakaryoctes (gigantic cell that forms without cell divison)
C. Platelets fragment from the megakaryocyte
Arrythymia & Examples
Irregular Heart Beat
Examples:
- Ventricular Fribulation= weak rippling contraction of ventricle
- Atrial Fribulation = weak rippling contraction of atria
- Heart Block = failure of any part of conduction system to conduct signals. Example: bundle branch blokc results from damage to one or both branches of the AV budnle which can lead to blocked signals from atria to ventricle and thus no venricular contraction.
- Premature Ventricular Contraction: Extra systole- firring of an extra beat.
Ventricular Fribulation
- Most widley known
- Weak rippling contraction in the atria
Pressure & Fluid Flow
Movement only occurs with pressure gradient: from high to low
Pressure and volume relationship
Inversely related
Pressure & Heart Valves
Opening & Closing are governed by pressure. They are passively pushed open and closed by the changes in blood pressure on the upstream and downstream sides of the valve.
When ventricles are relaxed and pressure is low- AV valve cusps hand down limply and valves are open. Blood flows freely from atria to ventricles even before atria contract.
As ventriles fill with blood, the cusps floar upwared toward the closed position. Once ventricle contract, pressure increases even more and valves seal tightly
Congestive Heart Failure
Fluid accumulation in either the pulmonary or systemic circuit due to insufficiency of ventricle pumping.
Causes: myocardial infarction, chronic hypertension, valvular defects, and congenital defects.
3 Vessel Layers
- Tunica Interna
- Tunica Media
- Tunica Externa
Vaso Vasorum
Smaller blood vessels supplying larger one
Supply blood to at least the outer half of the vessel wall (within the tunic externa)
*Tissues within the inner half of the vessel are likely supplied by diffusion from the lumen
Tunica Interna: Structure & Function
Lines inside of the vessel
Consists of simple squamous epithelium (endothilium)
Lining is selectively permeable
Secretes chemicals to influence vasodialation and vasoconstriction
Smooth lining prevents blood cells and platelets from congregating/ sticking to walls
Tunica Media: Structure & Function
Middle layer of blood vessel
Consists of smooth muscles, collagen, and elastic tissue
Smooth muscle & elastic tissue vary between vessels
Tunica Media strengthens vessels and prevents bp from rupturing the vessel
Also regulates the diameter of the vessel
Tunica Externa: Structure & Function
Outermost layer
Consists of loose connective tissue that merges with other blood vessels, nerves, or other ogans
Anchors vessels to adjacent tissues and provides passage for small nerves, lymphatic vessels, and smaller blood vessels
Why are arteries called resistance vessels ?
Have strong, resilient tissue structure that can withstand heavy loads of blood and pressure
They are more muscular than veins and can retain their shape when empty
3 Types of Arteries
- Conducting (elastic or large) arteries:
- Distributing (muscular or medium) arteries
- Resistance (small) arteries
Conducting (elastic or large) Arteries: Structure & Function
The largest
Has tons of elastic tissue
They expand when they recieve blood during ventricular systole and recoil during diastole
Examples: aorta, common caratid, subclavian, pulmonary trunk, common iliac
Arteriosclerosis
Stiffening of arteries (usually with age)
Protective effect of arteries weaken and downstream vessels are subjected with greaer stress and risks of aneurysm and hemorrhage rise
Distributing (muscular or medium) Arteries: Structure & Function
Smaller branches of arteries that supply blood to specific arteries
Compared to exit ramps where as conducting arteries are interstate highways
These arteries have a ton of muscle (more than elastic tissue)
Example: femoral, brachial, renal, and splenic
Resistance Arteries: Structure & Function
Most muscle to elastic tissue ratio
Thicker tunica media in proportion to lumen
Example: Arterioles
Metaarteriales
Link arterioles directly to venules
Provide shortcuts through which blood could bypass capillaries
Lymphatic System Functions
- Fluid Recovery
- Immunity
- Lipid Absorbtion
Transport Maximum
- The amount of solute that renal tubules can reabsorb is limited by the number of transport proteins in tubule cells’ membranes
- If all transporters are occupied, any excess solute passes by and appears in urine
- Transport maximum is reached when transporters are saturated
- Each solute has its own transport maximum
–Any blood glucose level above 220 mg/dL results in glycosuria
