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BIOL 273 Human Physiology 1 > Unit 4 Circulatory System > Flashcards

Unit 4 Circulatory System Flashcards

1
Q

what is the solution to diffusion limitation

A
  1. cardiovascular system for transport of substances through the body
  2. transported by flow of blood through circulatory system
  3. bulk flow rather than diffusion
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2
Q

what are the components of the circulatory system

A

-heart
-blood vessels
-blood cells and plasma

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3
Q

external anatomy of the heart

A

Pericardium
-tough membranous sac surrounding the heart
-made up of two layers with small amount of fluid between them that acts as a lubricant
Coronary Arteries
-supplies blood to the heart
-nourish the heart muscle
-heart has a very high oxygen demand (absolutely depends on adequate blood flow)
-lack of blood supply to heart leads to a heart attack

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4
Q

left atrium

A

-receives blood from the pulmonary veins
-sends to left ventricle

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5
Q

left ventricle

A

-receives blood from left atrium
-sends blood to body via aorta

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6
Q

right atrium

A

-receives blood from the venae cavae
-sends to right ventricle

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7
Q

right ventricle

A

-receives blood from the right atrium
-sends blood to the lungs via the pulmonary artery

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8
Q

valves

A

-ensure flow is unidirectional
-no valves at entrance to the right and left atria
-due to weak atrial contraction relative to ventricular contraction
-atrial contraction compresses the veins at the entry to the heart –> closes the exit to the heart and reduces backflow

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9
Q

Av valves

A

-tricuspid (right)
-bicuspid/ mitral (left)
- Attached on ventricular side to collagenous cords –> chordae tendineae (prevent valves from being pushed back into atrium)

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10
Q

Semilunar valves

A
  • aortic and pulmonary
  • Just inside aorta and pulmonary arteries –> prevent backflow into ventricles
  • The semilunar valves do not need cords to brace them because of their shape
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11
Q

what is the path of blood flow

A
  • Blood travels through the body in the cardiovascular system that consists of two divisions:
  1. Pulmonary circuit –> blood vessels in the lungs and those that connect the lungs to the heart
    - Blood flows from right atrium to right ventricle –> pumped to pulmonary arteries to the lungs
    - Lungs have many small capillaries to increase O2 transfer (small radius, high surface area –> increase resistance –> decrease pressure of blood)
    - Oxygenated blood has low pressure > need to return to heart via pulmonary veins to left atrium
  2. Systemic circuit –> encompasses the rest of the blood vessels in the body
    - Blood flows from left atrium to left ventricle –> pumped to aorta that branches into smaller arteries and then to capillary networks throughout the body
    - O2 diffuses from the blood into the tissues in the capillary beds –> then flow to small venules and then larger veins
    - Oxygen-poor blood has low pressure –> need to return to heart via superior vena cava and inferior vena cava to the right atrium
    - The heart increases the pressure of the blood at critical points in the double cycle
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12
Q

specialized cells in the heart

A
  • The heart is very different from other muscles
  • It does not require input from the nervous system for contraction
  • Heart contains specialized cells called autorhythmic cells (pacemaker cells)
  • Located in sinoatrial node (SA node) –> fastest to create action potential
  • Right atrium, near superior vena cava
  • Spontaneously generate action potentials without input from the nervous system
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13
Q

pacemaker potential

A
  • Pacemaker cells have an unstable membrane potential that slowly drift upwards from a starting point of -60 mV (pacemaker potential) until reaches threshold and initiates an action potential
  • Unstable membrane potentials because they have different membrane channels than other excitable cells
  • Special If channels (I stands for current, f stands for “funny” channels)
  • Permeable to K+ and Na+
  • all channels are voltage gated
  • When membrane potential is negative:
    Na+ influx > K+ efflux –> net influx of + charge –> slow depolarization of the membrane
  • When membrane potential goes towards positive (i.e. less negative):
  • If channels close; Ca2+ channels open –> continued depolarization –> threshold reached –> many Ca2+ channels open and rapid influx of Ca2+ –> steep depolarization phase of action potential
  • At end of depolarization the Ca2+ channels close and K+ channels open slowly; efflux of K+ causes repolarization
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14
Q

What is a major difference between action potentials and pacemaker potentials in the pacemaker cells?

A

Na+ and Ca2+ influx for pacemaker potential; only Ca2+ influx for action potential

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15
Q

modulation of the heart

A
  • The autonomic division modulates RATE of pacemaker potentials

a. Norepinephrine released from sympathetic neurons & Epinephrine released from adrenal medulla –> bind to beta 1 adrenergic receptor
- Release of cAMP through signalling pathway which binds to open Ir channels –> channels stay open longer –> increased permeability to and Na+ and Ca2+
- Increased depolarization rate which increases rate of action potentials –> heart rate increases

b. Acetylcholine released from parasympathetic neurons –> binds to muscarinic receptors
- Increases K+ permeability which hyperpolarizes the cell –> pacemaker potential starts at more negative value therefore it takes longer to reach threshold potential –> heart rate decreases

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16
Q

electrical communication in the heart

A
  • Pacemaker/autorhythmic cells initiate the electrical excitation of the heart
  • Depolarization spreads to neighbouring cardiac cells via gap junctions in the intercalated discs
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17
Q

events of conduction

A
  1. Action potential fired from SA node
    –> spreads to adjacent cells
  2. Rapid spread through cells of
    internodal pathway
    - Spread is slower through contractile cells of atrium (WHY?) –> cytoplasmic resistance (lots of material inside cell)
  3. Signal passed through AV node ONLY at AV junction. A layer of fibrous connective tissue (fibrous skeleton of
    the heart) acts as insulator prevents electrical signals from atrium to the ventricle
    -Therefore, AV node ONLY pathway for action potential
    -Signal is slightly delayed by AV node to make sure that the atria have finished contracting
  4. Signal is carried to bottom of heart through bundle of His (AV bundle)
  5. Bundle of His divides into left and right branches –> Purkije fibres transmit signals VERY rapidly to ensure that all the contractile cells at the apex contract together
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18
Q

why is it necessary to conduct signals only through the AV node and bundle of His

A

-want signal for contraction to start at the bottom of the heart
-ensures the contraction drives the blood up since it exits the heart at the top

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19
Q

what is the electrocardiogram

A
  • Use electrocardiogram (ECG/EKG) to obtain information about the heart
  • Action potentials trigger the contraction of both atria at about the same time and of both ventricles a ‘split’ second later
  • Record the electrical activity at the surface of the skin using electrodes
  • Measure the voltage differentials occurring during the cardiac cycle –> single contraction-relaxation of the mechanical events
  • Use 3 leads to make up “Einthoven’s triangle”
  • Nowadays clinically use 12 ECG leads –> gives information about different regions of the heart
20
Q

what are the components of the ECG

A
  1. Waves
    - Deflections above or below the baseline
    - Electrical events
    3 major waves:
  2. P wave –> depolarization of atria
  3. QRS complex –> ventricular depolarization
  4. T wave –> repolarization of ventricles
    *atrial repolarizationis masked by QRS complex
  5. Segments
    - Sections of baseline between two waves
    - Mechanical events, lag slightly behind electrical events
    - 2 segments (baseline between waves):
  6. P-R segment –> atrial contraction
  7. S-T segment –> ventricular contraction, just after Q wave
    - ECG provides information such as heart rate (timed from P wave to P wave)
21
Q

phases of the cardiac cycle

A
  • The cardiac cycle is the period from one heartbeat to the next and has two phases:
    1. Systole - contraction
    2. Diastole-relaxation
  • Steps to cycle:
    1. Late diastole: atria and ventricles are relaxed –> semilunar valves closed; AV valves open –> blood enters ventricles passively
    2. Atrial systole: atria contract, ventricles relaxed –> semilunar valves closed, AV valves open –> small amount of blood enters ventricles
    3. Isovolumic ventricular contraction: ventricles contract –> AV and semilunar valves closed
    4. Ventricular ejection –> semilunar valves open, AV valves shut –> blood ejected
    5. Isovolumic ventricular relaxation –> semilunar valves closed; AV valves closed
    6. Go back to Step #1
  • Normal heart makes two main sounds (lub-dub) during the cardiac cycle:
    i. “lub” –> due to closing of AV valves (step 3 above)
    ii. “dub” –> due to closing of semilunar valves (step 5 above)
22
Q

pressure volume relationships

A
  • Liquids & gases flow from higher pressure areas to areas of lower pressure
  • Heart contracts the pressure increases blood flows out of the heart to lower pressure areas
  • End Diastolic Volume (EDV) –> maximum volume in ventricle - end of ventricular filling
  • End Systolic Volume (ESV) –> minimum volume in ventricle - end of ventricular contraction
23
Q

calculate cardiac output

A

cardiac output= heart rate x stroke volume
stroke volume = EDV - ESV

24
Q

factors that influence heart rate

A
  1. Parasympathetic Stimulation –> decreases heart rate
    - Via vagus nerve –> ACh
  2. Sympathetic Stimulation –> increases heart rate
    - Via great cardiac nerve –> NE
  3. Plasma Epinephrine (from adrenal medulla) –> increases heart rate
25
Q

factors that influence stroke volume

A
  1. Parasympathetic Stimulation –> decreases contractility
  2. Sympathetic Stimulation –> increases contractility
  3. Plasma Epinephrine –> increases contractility
  4. Increased End-Diastolic Volume –> increases stroke volume
26
Q

factors affecting venous return

A
  1. Total blood volume –> more blood means more can be loaded into the ventricles
  2. Sympathetic vasoconstrictor nerves –> constrict blood vessels pushes blood toward the heart
  3. Skeletal muscle pump –> muscle contractions push blood toward heart
  4. Respiratory pump –> creates low pressure in thorax and high pressure in abdomen
27
Q

structure of blood vessels

A
  • Hollow tube made up of:
    1. Lumen –> central Cavity
    2. Wall –> made of layers:
    a. Inner lining –> endothelial cells make up the endothelium
    b. Elastic connective tissue
    c. Vascular smooth muscle
    -Vasoconstriction –> narrowing of the vessel
    -Vasodilation –> widening of the vessel
    d. Fibrous connective tissue
  • not all blood vessels have all layers
28
Q

types of blood vessels

A

a. Artery - thick walled to withstand high pressure (all 4 layers)
b. Arteriole - smallest arteries (layer a and c)
c. Capillary - smallest blood vessel –> exchange of material (only layer a)
d. Venule - smallest veins (layer a +d)
e. Vein - transport blood at low pressure (all 4 layers)

29
Q

blood flow and pressure

A
  • Blood flows because of a pressure gradient (delta P) between the arteries (P1 - highest) and veins (P2 - lowest)
  • Flow is directly proportional to the pressure gradient
  • There are factors that influence blood flow through the vessels of the body:
  1. Myogenic autoregulation (vascular smooth muscle) –> stretch receptors in wall of arterioles when activated cause vasoconstriction
  2. Paracrine hormones –> released from vascular endothelium and tissues
    - Cause vasodilation or vasoconstriction
  3. Innervation by sympathetic division of autonomic nervous system
    - Norepinephrine –> binds to alpha receptors, causes vasoconstriction
    - Epinephrine –> binds to alpha receptors, reinforces vasoconstriction
  4. Hormonal Signals via circulating epinephrine –> binds to Beta 2 receptors
    - Found ONLY in vascular smooth muscle of heart, liver (stores glycogen), and skeletal muscle arterioles
    - Causes vasodilation in blood vessels
    giving blood to muscle of heart
30
Q

how does resistance oppose flow

A
  1. Pressure is increased when volume decreases (volume of the vessel, not the amount of liquid inside the vessel)
    - In the circulatory system the heart generates pressure by contracting
    - Contract (decrease volume) –> increase pressure
  2. Pressure is decreased by friction
    - Friction is the force that resists relative motion between two bodies in contact
    - In the circulatory system, friction occurs between blood and the walls of the blood vessel
    - Friction exerted by a tube is generally called its resistance
  • Described mathematically for fluid flowing through a tube: R = 8Ln/pi*r^4
    where: L = length of the tube
    n= viscosity of the fluid
    r= radius of the tube
  • In the human circulatory system L and n are generally almost constant
  • Adjustments are made by changing r (radius of blood vessels)
  • Flow is inversely proportional to resistance
  • Since flow is proportional to the pressure difference and inversely proportional to the resistance: Flow is proportional to the pressure difference over the resistance
31
Q

a small change in
which factor will have
the greatest effect on resistance?

A

radius

32
Q

summary of blood flow and resistance

A

a. Blood flow only occurs when there is a pressure gradient
- From high –> low pressure
b. Resistance (R) decreases flow of the blood
- Determined by length, radius, and viscosity: changes in radius are the most important under normal physiological conditions
c. Flow is proportional to the pressure difference over the resistance

33
Q

blood pressure

A
  1. Arterial blood pressure reflects the driving pressure caused by the heart pumping
    - Highest in arteries
    - Lowest at point of return to the heart
    Your pulse is an increase in pressure caused when ventricles contract and push blood into aorta
  2. Two parts make up blood pressure
    a. Systolic pressure: time when the heart is contracting –> highest arterial pressure
    b. Diastolic pressure: time when the ventricle relaxes –> lowest arterial pressure
  3. Estimation of blood pressure is done by sphygmomanometry –> use of blood pressure cuff & stethoscope
  4. Mean arterial pressure (MAP) –> since arterial pressure is pulsatile use a single value to represent driving pressure
    Mean Arterial Pressure = diastolic P + 1/3 (systolic P - diastolic P)
  5. Factors affecting Mean Arterial Pressure:
    a. Cardiac output
    b. Changes in blood volume (under normal circumstances this is constant!)
    c. Peripheral resistance
    - Largely controlled by arterioles which have large amounts of smooth muscle in their walls –> can modify the diameter
    - Small changes in radius –> large changes in resistance
    - Influenced by both reflex & local control mechanisms
34
Q

what are the steps of sphygmomanometry

A
  • Steps:
    1. Inflate cuff –> cuts off blood flow
    2. Cuff is gradually deflated, when pressure in cuff = systolic pressure –> blood will start to flow
    3. Turbulent flow results in sound –> Korotkoff sound (with each heartbeat)
    4. Cuff pressure further reduced
    5. Eventually all sound will cease because flow is no longer turbulent –> diastolic pressure
35
Q

how is blood pressure regulated

A

Coordinated by CNS –> a homeostatic reflex
- Blood pressure is monitored through sensory input from baroreceptors –> these are stretch sensitive mechanoreceptors found in vessel walls of the:
- Carotid artery –> monitors blood pressure to brain
- Aorta –> monitors blood pressure to body
- Baroreceptor reflex based an increase in blood pressure from normal (i.e., initial pressure is high)
1. Membrane of baroreceptor stretches
2. Increases firing rate of receptor
3. Action potentials travel to cardiovascular control centre in CNS (medulla)
4. Control centre integrates the sensory input
5. Efferent output carried by autonomic neurons
6. Decrease in sympathetic output & increase in parasympathetic output
Causes:
- Vasodilation
- Decrease in force of cardiac contraction and heart rate
- Decrease in peripheral resistance and cardiac output
7. Result is a decrease in blood pressure

36
Q

what is blood made of?

A
  • Blood is the circulating component of extracellular fluid responsible for carrying substances around the body
  • 4 major components:
    1. Plasma –> fluid portion of the blood
  1. Red blood cells –> erythrocytes
    - Biconcave in shape
    - Most abundant cells in blood
    - Contain protein haemoglobin
    - Major function of erythrocytes is gas (O2 and CO2) transport
    - In humans (mammals), RBCs lack a nucleus & mitochondria –> rely on glycolysis
  2. White blood cells –> leukocytes
    - WBCs function in immune responses
    i. Lymphocytes
    il. Monocytes (macrophage)
    ili. Granulocytes –> 3 types
    - Neutrophils
    - Eosinophils
    - Basophils (mast cells)
    - Macrophages and neutrophils are the professional phagocytes in the body
  3. Platelets –> thrombocytes
    - Involved in blood clotting
    - Derived from megakaryocytes –> pinch off and have no nucleus
37
Q

haemoglobin synthesis

A
  • Synthesis of haemoglobin is required for RBC function to transport oxygen
  • Large complex molecule made up of 4 protein chains (globins)
  • Each globin subunit is wrapped around an iron containing haeme group
  • Haeme group C-H-N porphyrin ring contains an Fe in the centre
  • Hemoglobin synthesis requires adequate dietary iron –> low dietary iron can result in anemia (decreases oxygen carrying capabilities)
38
Q

haemoglobin binding

A

-A variety of factors can affect haemoglobin-O2 binding which alter the configuration of haemoglobin –> thus it alters the properties of haemoglobin
- This is a form of allosteric modification
- e.g. temperature, pH
- Increases in temperature decrease haemoglobin-oxygen affinity
- Increases in blood CO2 and H+ decrease haemoglobin-oxygen affinity
- A shift in haemoglobin saturation due to pH is called the Bohr effect
- All these factors are elevated in the tissues relative to the lungs –> higher temp, PCO2 and H+ (higher levels)
- This leads to O2 unloading at the tissues
- The more active a tissue the greater the increases in PCO2, H+ and temp
-Therefore, more O2 is released

39
Q

what is haematopoisis

A
  • Broken down into its root words: Haima = blood; Poiesis = formation
  • All blood cells are produced in the red bone marrow
  • Arise from a single precursor –> pluripotent haematopoietic stem cell
  • Can develop into many
    different cell types as the
    cells develop through a
    series of stages
  • Uncommitted stem cells still capable of many fates
  • Progenitor cells are committed to one or two cell types
  • Path taken is guided by
    cytokines –> small peptides/proteins secreted by one cell to send signals to another
    -Often called factors with a modifying word describing their action (e.g. growth factor, modifying factor)
40
Q

Leukopoiesis

A
  • Formation of leukocytes (white blood cells) that is regulated by the colony-stimulating factors (CSFs)
  • CSFs are released by endothelial cells, marrow fibroblasts & white blood cells
  • Induce cell division and cell maturation in stem cells
    -Cytokines released by leukocytes regulate further leukocyte production
  • e.g. if you have an active bacterial infection –> cytokines that are released will result in production of more macrophages & neutrophils to help fight the infection
41
Q

thrombopoiesis

A
  • Megakaryocytes are parent cells that produce platelets (thrombocytes)
  • Growth and maturation are regulated by cytokine thrombopoietin (TPO)
  • Cells undergo mitosis up to 7 times without undergoing nuclear or cytoplasmic division
  • Megakaryocyte is a polyploid cell with a lobed nucleus
  • The megakaryocyte resides in the bone marrow and extends its outer edges through the endothelium (cells lining the blood vessels) into blood stream
  • The ends fragment into disk-like platelets which have no nucleus, but contain mitochondria, smooth ER and granules filled with clotting proteins and cytokines
  • Platelets are always present in the blood –> not active unless damage has occurred to the walls of the circulatory system
  • about 10 day life span
42
Q

erythropoiesis

A
  • Formation of red blood cells
  • Regulated by erythropoietin (EPO) –> commonly called a hormone but it is a cytokine
  • EPO is a glycoprotein made primarily in the kidneys
  • EPO synthesis and release is regulated by hypoxia (low O2)
43
Q

what is haemostasis

A
  • Haima = blood; Stasis = stoppage
  • Prevents blood loss from damaged vessels –> need to maintain the integrity of the blood vessels
  • The flow of blood throughout the body cannot be turned off to fix a leak
    Flow cannot even be turned off locally or cells will die –> must be fixed under pressure (literally)
  • If the patch is too weak it will be blown off
44
Q

what are the steps of haemostasis

A
  1. Vascular spasm –> like putting pressure on a bleeding wound
    - Via vasoconstrictive paracrines released by damaged endothelium of the blood vessel
    - Decreases blood flow by increasing resistance –> Promotes formation of platelet plug
  2. Platelet plug to temporarily block break
    - Collagen (activates platelets) is normally in the sub-endothelial layer –> platelets stick & become activated
    - Releases cytokines –> activate more platelets
    - Activated platelets stick together (aggregation) to form a loose platelet plug –> this slows blood flow in the vessel & provides a framework for clotting (step #3)
  3. Blood clot to seal the break –> this is a result of the coagulation cascade
    - Inactive plasma proteins are activated by either exposure to factor XII to collagen (intrinsic pathway) or exposure to tissue factor III (extrinsic pathway) released from damaged cells
    - There are several steps in each pathway (intrinsic and extrinsic) which involve protein factors that are turned on to activate the next protein factor in the pathway
    - Both pathways merge into the common pathway and lead to the activation of thrombin which cleaves fibrinogen into fibrin
    - Thrombin also activates factor XIII which cross-links the fibrin into long fibres that intertwine to form a fibrin network
    - Intertwined fibres reinforce the platelet plug making it a clot
    - Excessive clotting produces a thrombus –> a clot which can block blood vessels
45
Q

healing after a break

A
  • During clot formation plasminogen is converted into plasmin by either thrombin or tissue plasminogen activator (tPA)
  • The enzyme plasmin dissolves the clot –> fibrinolysis
  • As repairs progress, the clot slowly shrinks

BIOL 273 Human Physiology 1 (6 decks)

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