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Cardiovascular System - Intro to the Heart
Pyramid Comparison
apex and base
top is apex (most narrow), base is widest portion
heart has base at top (widest portion)
heart has apex at bottom (points down and towards the left)
centered within the body, but skewed pointing towards the left (on patient)
Arteries
carries blood away from the heart
Veins
carries blood towards the heart
Location
located within the mediastinum
middle of body, sandwiched between left and right lung
on superior surface of diaphragm
anterior to vertebral column
posterior to sternum
medial to left and right lung


Heart Structure
2 types of chambers, 4 total
atria (plural) → upper chambers
right and left atrium
ventricles (plural) → lower chambers
right and left ventricle
chambers that blood flows through
surrounded by living tissues
blood flowing through chambers is not what nourishes the heart tissues
coronary circulation → blood vessels that nourish the heart
2 pumps
act at same time, but supply blood to different portions
atria go to ventricles
leaves from ventricles to other locations
blood comes in the left atrium and go to left ventricle
contraction happening for both sides and blood coming into atria at same time (one drop of blood flows at different times though)

Pulmonary and Systemic Circuits
heart transport system; two side-by-side pumps
right side 1. receives oxygen-poor blood from tissues (into pulmonary circuit)
right side (ventricle contracts to pump blood to lungs)
sent through artery to lungs to get oxygenated
brings O2 rich blood to left side of heart
pumps to lungs to get rid of CO2, pick up O2
pulmonary circuit
left side 2. receives oxygenated blood from lungs (into systemic circuit)
left side (ventricle contracts to pump blood to body tissues)
travels through artery to tissues
delivers O2 and picks up CO2 and returns to other side of heart
pumps to body tissues
systemic circuit

Asymmetry of Ventricles
most of the time, the body is symmetrical
ventricles differ in symmetry
myocardium differs between both sides of the heart
left ventricle myocardium is much thicker than right ventricle
explained by the fact that the left ventricle must contract with a greater force to push blood to body tissues, while right ventricle must only contract enough to push blood to the lungs (shorter distance away = less force required to move)
contraction increases pressure (heart becomes smaller = higher pressure)
pumping blood to tissues requires more pressure and force (lower extremities less so, because gravity will pull blood down, however, upper extremities means blood must push against gravity)
Heart Form and Function
myocardium (muscles of the heart)
left ventricle - 3x thickness of myocardium compared to right side


Layers of the Heart Wall
Three layers of heart wall
epicardium → visceral layer of serous pericardium
innermost layer (visceral) of pericardium and outermost layer of heart
count as one of the same, not two separate layers
myocardium
contractile cardiac muscle cells
cardiac skeleton: crisscrossing, interlacing layer of connective tissue
anchors cardiac muscle fibers
supports greater vessels and valves
limits spread of action potentials to specific paths
only goes through certain pathways at specific times
coordinates contractions
endocardium → lines heart chambers and valves
continuous with blood vessels
helps reduce friction of blood against vessel walls
ensures continuous flow
Pericardium
deep two-layered serous pericardium
parietal layer
visceral layer (epicardium)
separated by fluid-filled pericardial cavity

Septum
interatrial septum → separates atria (in-between atria)
inter ventricular septum → separates ventricles (in-between ventricles)
divides atria and ventricles between themselves
Valves
unidirectional
pressure → open and close
areas of high pressure
opens one side and closes other side
pressure in atria → opens
pressure in ventricle → slams valve closed
open with high pressure on one side and closes with high pressure on other side
two atrioventricular (AV) valves
tricuspid valve (right)
mitral/bicuspid valve (left)
papillary muscles; chordae tendinae
chordae tendinae → strings that anchor into muscles within wall of heart (anchors into papillary muscles) and hold AV valve in place, preventing it from flipping and inverting
left atrium (bicuspid valve), right atrium (tricuspid valve)
two semilunar (SL) valves (blood leaving the heart)
aortic semilunar valve (left ventricle → aorta → systemic circuit)
pulmonary semilunar valve (right ventricle → pulmonary circuit)
AV Valves
blood returns to heart, filling right atria, pressing against AV valves = increased pressure forces AV valves open
as ventricle fills, AV valve flaps hang limply into ventricle
atria contracts, forcing additional blood into ventricles
ventricles contract, forcing blood against AV valve cusps
AV valve closes
papillary muscle contracts and chordae tendinae tighten, preventing valve flaps from everting into atria
Semilunar Valves
closes because blood falls back down on it, causing it to close
REVIEW AND ADD
Daily Question - Heart Sounds
normal heart sounds → valves closing (two sounds, because two different periods that valves close)
AV closing, semilunar closing (repeats after pause), producing beating heart sound
two sounds (Lub-dup) associated with closing of heart valves
first as AV valves close (lup)
second as SL valves close (dup)
heart murmurs → abnormal heart sounds; usually indicate incompetent or stenotic valves
mitral (bicuspid) valve regurgitation
Pathway of Blood
Pulmonary Circuit
right atrium → tricuspid valve → right ventricle
right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs
lungs → pulmonary veins → left atrium
Systemic Circuit
left atrium → mitral valve → left ventricle
left ventricle → aortic semilunar valve → aorta
aorta → systemic circulation (body tissues)
superior vena cava → inferior vena cava → right atrium → right ventricle → pulmonary SL valve → pulmonary artery (right and left pulmonary arteries deliver to right and left lungs) → lungs → pulmonary vein (high oxygen) → left atrium → mitral valve → left ventricle → aortic semilunar valve → aorta → body tissues
large quantity of blood just drops down from gravity, but other portion comes from heart muscles contracting (makes high pressure environment)
as ventricle fills with blood, tricuspid valve then closes (pressure builds)
high pressure environment within right ventricle triggers pulmonary SL valve to open
shoots up with a lot of force and slams back down, closing the pulmonary SL valve
right ventricle no longer high pressure = tricuspid valve reopens
oxygen picked up within lungs and brought back to heart through pulmonary vein
two vessels (pulmonary right and left veins) connect to left atrium
mitral AV valve open from higher pressure of blood filling atrium, blood enters left ventricle → pressure increases in ventricle, closing mitral valve and opening aortic semilunar valve → aorta
Microscopic Anatomy of Cardiac Muscle
Intercalated discs
desmosomes → lock cells in place; when mechanical force present, keeps cells together
gap junctions → electrically couple cells (ions flow between cells, electrically linking cells together)
allows heart to be functional syncytium
all cardiomyocytes contract as a unit, or none do
ensures larger force of contraction (required for ventricle to get high pressure environment for blood to eject out)
enables coordinated contractions
99% contractile. 1% auto-rhythmic
contractile → contract because neighbor contracts (neighbors pass messages to contract between each other → electrically coupled cells)
auto-rhythmic → start message for contraction that radiates out to other cells


Action Potentials - Muscle Contraction
graph = time vs membrane potential
rest = -70 mV (inside cell is more negative than environment)
higher concentration sodium ions outside cell compared to inside and lots of potassium inside compared to outside
depolarization = sodium ions come in to cell (cell becomes more positive than environment) = membrane potential increases = action potential → potassium ions begin to leave (depolarization) = becomes more negative than environment and even more negative than rest → hyper-polarization → resting membrane potential
Heart
many electrical messages being sent
pathway for signaling contraction:
sinoatrial node → located in right atrium and contain auto-rhythmic cells
all around auto-rhythmic cells = contractile cells = messages spread out across cells
interatrial bundle (Bachman’s bundle or interatrial tract)
connecting sionatrial node to right atrium, triggering depolarization to spread in the right atrium and left atrium
internodal tract → connects atrioventricular node to right atrium
auto-rhymthic cells
0.1 seconds later (pause → diameter changes in node = slower travel through tracts)
benefit: whole heart contracts at once without this delay
pause ensures that atria contract slightly before ventricles do = ensures atria receive message first = more atria in blood = more blood enters ventricles
continues down atrioventricular bundle (bundle of His) → splits into left and right bundle branches → splits into purkinje fibers (subendocardial conducting network) → spread throughout myocardium of ventricles
auto-rhythmic cells around purkinje fibers
auto rhythmic cells in both AV node and SA node → ensures that if a message isn’t sent out from SA node or AV node doesn’t receive message = ensures another place where this contraction messaging could occur
backup mechanism to ensure ventricles contract
summary: Sinoatrial node → Atrioventricular node → Atrioventricular bundle → Right and left bundle branches → Subendocardial conducting network (Purkinje fibers)


Cardiac Action Potentials
cardiac action potentials slightly different shape and Ca2+ plays a role
electrical message occurs → activates Ca2+ release → actin and myosin cross-bridge formation → contraction occurs in muscle
Contractile Muscle Cells
resting state = negative membrane potential
stimulus occurs = depolarization → Na+ influx through fast-voltage gated Na+ channels
positive feedback cycle rapidly open many Na+ channels, reversing membrane potential. channel inactivation ends phase
plateau phase → Ca2+ influx through slow Ca2+ channels. this keeps the cell depolarized, because few K+ channels are open
calcium slows return to more negative state
repolarization
due to Ca2+ channels inactivating and K+ channels opening. this allows K+ efflux, which brings membrane potential back to resting voltage.
Pacemaker Cells (auto-rhythmic)
pacemaker potential → slow depolarization due to both opening of Na+ channels and closing of K+ channels. membrane potential is never flat line
depolarization → action potential begins when pacemaker potential reaches threshold. depolarization due to Ca2+ influx through Ca2+ channels
repolarization → due to Ca2+ channels inactivating and K+ channels opening. this allows K+ efflux, which brings membrane potential back to most negative charge


Electrocardiography
electrocardiogram (ECG or EKG)
all action potentials at given time
three waves:
P wave → depolarization of SA node → atria
atrial cells become very positive
QRS complex → ventricular depolarization and atrial depolarization
atrial cells become very negative
ventricular cells become very positive
T wave → ventricular repolarization
ventricular cells become very negative
Missing Image:
Q is missing
labels don’t change when things are missing


ECG vs Heart
no P wave = SA node blocked
AV node still depolarizes = signals atria to still contract, ventricles are still contracting, but less blood present
erratic signals = electrical signals still receiving messages, but muscles are contracting uncoordinated = blood not ejected from heart correctly = fibrillation (heart attack or electrical signal)

Mechanical Events: Cardiac Cycle
systole = contraction
diastole = relaxation
cardiac cycle
Blood flow through heart during one complete heartbeat
Atrial systole and diastole → ventricular systole and diastole

Phases of Cardiac Cycle
Ventricular Filling
AV valves are open; pressure low
80% of blood passively flows into ventricles
Atrial systole occurs, delivering remaining 20%
End diastolic volume (EDV) → volume of blood in each ventricle at end of ventricular diastole
once ventricle is filled, before contraction occurs
at very end of relaxation phase of heart
volume in a single ventricle (about the same between left and right)
Ventricular Systole
atrial diastole; ventricles begin to contract
isovolumetric contraction phase (closed valves)
ventricular pressure > artery pressure
blood moves from high pressure to low pressure
big difference = more blood moved faster
End systolic volume (ESV) → volume of blood remaining in each ventricle after systole
no matter how strong contraction is, some blood stays within the ventricle
how much blood is in a single ventricle after ventricular systole (contraction)
Isovolumetric Relaxation
ventricles relax; atria relaxed and filling
blood closes SL valves
AV valves open; cycle begins again at step 1
Juice Box Analogy
Jug = atria
1st straw = AV valve/pathway to ventricle
Juice Box = ventricle
2nd straw = artery
Total Blood Volume Output = End diastolic volume - end systolic volume
Impacts on Blood Out:
Force of contraction
How much filled
Cardiac Output

Cardiac Output (CO)
volume of blood pumped by each ventricle in one minute
CO = heart rate (HR) * stroke volume (SV)
HR = number of beats per minute
SV = volume of blood pumped out by one ventricle with each beat
Normal - 5.25 L/min
CO (ml/min) = HR (75 beats/min) * SV (70 ml/beat)
= 5.25 L/min
SV DOESN’T equal end diastolic volume
TPS: If we have 100 ml of blood in a ventricle prior to contraction and 10 ml remained in the ventricle after the contraction, then what is the stroke volume, end diastolic volume, and end systolic volume?
EDV = 100 ml
ESV = 10 ml
SV = 100 ml - 10 ml = 90 ml
SV = EDV - ESV
Cardiac Output Variation
CO increases if either/both SV or HR increase
maximal CO is 4-5 times resting CO (~25 L/min)
up to 35 L/min in trained athletes
Cardiac reserve → difference between resting and maximal CO
Regulation of Stroke Volume
SV = EDV - ESV
EDV → length of ventricular diastole & venous pressure
ESV → arterial BP & ventricular contraction strength
Three main SV impactors:
preload
contractility
afterload
Preload
degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of heart)
venous return → amount of blood returning to heart
increased venous return distends (stretches) ventricles
Contractility
contractile strength
Increased Contractility
sympathetic stimulation → increased Ca2+ influx → more cross bridges
Decreased Contractility
calcium channel blockers = fewer cross bridges formed = weaker contraction
Afterload
pressure ventricles must overcome to eject blood
hypertension = increased after load = increased ESV = decreased SV
high pressure = larger hurdle to get over = less blood moves = higher ESV
high pressure → low pressure


Cardiac Output & Heart Rate
CO = heart rate (HR) * stroke volume (SV)
CO increases if either/both SV or HR increases
positive chronotropic factors = increase heart rate
negative chronotropic factors = decrease heart rate
Regulation of Heart Rate
Fear → sympathetic nervous system → epinephrine → B1 receptors of SA node (receptors on auto-rhythmic cells) → Na+ & Ca2+ (channels opened through receptor binding) → causes depolarization = message for contraction to be sent, if muscle works, it will contract (more action potentials) → increased heart rate & stroke volume
epinephrine → positive chronotropic factor
if administered clinically → chronotropic drug
Parasympathetic system returns heart rate to normal
Vagus nerve → ACh (interacts with auto-rhythmic cell in AV and SA nodes) → binds to M2 (muscarinic acetylcholine/cholinergic) receptors on SA node → opens K+ channels and closes Ca2+ channels (harder to reach peak = reaches peak less often = less action potentials) → decreased heart rate & stroke volume
Broad Factors Influencing Heart Rate
Age (size)
fetus has fastest HR
Sex (size)
Females faster than males
on average, females have lower body mass = higher HR
Exercise
increases HR
Body Temperature
HR increases with body temperature
Chemical Factors
Intra- and extracellular ion concentrations (ca2+ and K+)
Hypocalcemia (ca2+) → depresses HR
Hyper-calcemia (ca2+) → increases HR and contractility
Hyper-kalemia (potassium) → alters electrical activity, cardiac arrest
Hypokalemia (potassium) → feeble heartbeat, arrhythmia
Hormones
epinephrine from adrenal medulla increases HR and contractility
thyroxine enhances effects of norepinephrine and epinephrine (stronger impact of epinephrine → synergistic)

Heart Rate Regulation Summary
cardioacceleratory center → sympathetic nerve fibers (SS → epinephrine → B receptors → Na+ and Ca2+ channels → increased HR and stroke volume)
PS → vagus nerve → ACh → M2 receptors → opens K+ channels and closes Ca2+ channels → hyper polarized → decreased heart rate and decreased stroke volume
redundancy in innervating SA and AV nodes
other backups on purkinje fibers (can be chemically stimulated)
TPS:
SA node intrinsically fires 100/min
Typical resting HR: ~ 75 beats/min
Why difference?
Vagal tone → at rest, parasympathetic nervous system is more active than sympathetic nervous system = suppresses firing rate of SA node

Heart Rate Homeostatic Imbalances
tachycardia → abnormally fast HR (>100 beats/min)
if persistent, may lead to fibrillation
bradycardia → heart rate slower than 60 beats/min
may result in inadequate blood circulation
other factors might makeup for slower heart rate (venous return, lower blood pressure, etc)

Blood Flow Through Body
highway system with many exits (big highways lead to smaller exits = leads to smaller vessels, etc)
gets to capillaries = site of exchange
blood returns to heart going from smaller vessels → larger vessels
gets close to most cells of the body to deliver oxygen, nutrients, etc and then pickup waste, chemical messengers, etc
Impacts on Blood Flow
Vasodilators
low oxygen and increased carbon dioxide
Vasoconstrictors
Temperature
as temperature rises:
hypothalamus signals → warm blood flushes into capillary beds → heat radiates from skin (heat lost to environment = blood turns colder)
sweat also causes vasodilation via bradykinin in perspiration
more blood sent to site where blood is being cooled
as temperature decreases:
blood is shunted to deeper, more vital organs (avoids heat loss to environment)
blood goes to more vital areas of the body and less blood to areas with more contact with environment

ADD MISSING LECTURE

The Respiratory System
Major Function: Respiration
supply O2/remove CO2 associated with cellular respiration;
four processes associated respiratory and circulatory systems
Olfaction & Speech
odor molecules bind
speech → production of sound through force of air moving out of body
Purify, Humidify, and Warm Incoming Air
warm, clean, and make wetter

Processes of Respiration
Respiratory System
Pulmonary Ventilation
breathing → air in and out of lungs
external and internal environment interacting
External Respiration
O2 and CO2 between lungs and blood
movement within the lungs to the blood and blood to within the lungs
Circulatory System
Transport
O2 and CO2 in blood
Internal Respiration
O2 and CO2 between systemic blood vessels and tissues
Pulmonary Ventilation → Transport → External Respiration → Transport → Internal Respiration


Functional Zones
Respiratory Zone → site of gas exchange
microscopic structures
respiratory bronchioles, alveolar ducts, and alveoli
external respiration
Conducting Zone → conduits to gas exchange sites
all other respiratory structures;
cleanses, warms, and humidifies incoming air
dehumidifies air leaving (and reclaims heat)
Diaphragm and other respiratory muscles promote ventilation
Respiratory System - Functional Anatomy
Major Organs
nose, nasal cavity, and paranasal sinuses
pharynx
larynx
trachea
bronchi and their branches
lungs and alveoli
Upper Airways → Head & Neck (up to pharynx)
Respiratory Tract → Larynx to Lungs


The Nose
Two regions-external nose and nasal cavity
Functions:
Airway
Moisten and Warms entering air
respiratory mucosa
Filters and Cleans inspired air
respiratory mucosa & vibrissae (hairs)
Chamber to resonate speech
only certain sounds
sound still being produced, but not bouncing off chamber
Olfactory receptors
olfactory mucosa on superficial surface

Mucosa
Olfactory Mucosa
olfactory epithelium
Respiratory Mucosa
pseudo stratified ciliated columnar epithelium
mucous and serous secretions
inspired air warmed by capillaries and veins


Conchae
Nasal Conchae → superior, middle, and inferior
protrude medially from lateral walls
increase mucosal area
enhance air turbulence
Conchae and Nasal Mucosa
During Inhalation:
Filter, heat, and moisten air
During Exhalation:
Reclaim heat and moisture
Inhalation: Adding Obstacles/Protrusions to the Wall (lined with respiratory mucosa) → slow down things moving through the nose and force them to touch the walls of the structures to get cleaned, warmed, etc
Exhalation: Air takes heat and water, gets to lungs (warm, wet, clean), leave lungs (warm, wet, clean), on way back out - surfaces are colder (heat and water goes to lower concentration/colder), so reclaims heat and water


Paranasal Sinuses
cavities
in frontal, sphenoid, ethmoid, and maxillary bones
lighten skull; resonate sound; secrete mucus; help to warm and moisten air
Pharynx (Throat)
muscular passage
connects nasal cavity to larynx
three regions:
nasopharynx: superior region behind the nasal cavity
only air
air passes through this cavity if inhaled through nose
oropharynx: middle region behind mouth
food - digestive system
air - respiratory system
laryngopharynx: inferior region attached to larynx
food - digestive system
air - respiratory system

Larynx (Voice Box)
plays a role in speech
routes air and food into proper channels
eight rigid hyaline cartilages and spoon-shaped flap of elastic cartilage (epiglottis)


Larynx Structures
Epiglottis
routes food to the esophagus and air towards the trachea
Laryngeal Prominence
thyroid cartilage
adam’s apple
Vocal Folds (True Vocal Cords)
vibrate with expelled air to create sound (speech)
vestibular fold (false vocal cord)
Glottis
opening between vocal cords

Trachea (Wind Pipe)
Four-inch-long-tube
connects larynx with bronchi
Walls reinforced with C shaped hyaline cartilage
gives more plasticity
lined with pseudo stratified ciliated columnar epithelium
cilia beating creates a current that moves dirt/debris back towards external environment and away from lungs

Lungs
thoracic cavity
apex is near the clavicle (superior portion)
base rests on the diaphragm (inferior portion)
each lung is divided into lobes by fissures
left lung, two lobes
cardiac notch (where heart lies near lungs) is what gives left side only two lobes
right lung, three lobes


Bronchi
all but the smallest of these passageways have reinforcing cartilage in their walls
primary bronchi
secondary bronchi
tertiary bronchi
bronchioles
terminal bronchioles


Alveoli
alveoli = site of gas exchange
300 million alveoli/lung
rich blood supply-capillaries from sheet over alveoli
type I alveolar cells → most cells of the walls
make up wall of alveoli
single layer epithelial cells
type II alveolar cells
secrete surfactant


Alveoli and Surface Tension
surface tension: attracts liquid molecules to one another at gas-liquid interface
water → high surface tension (due to hydrogen bonds)
coats alveolar walls
surfactant → prevents alveoli from collapsing when we breathe out
lipid and protein complex produced by type II alveolar cells
reduces surface tension of alveolar fluid and discourages alveolar collapse
prevents water molecules from forming hydrogen bonds with other water molecules on opposite walls

Surfactant Image
contains hydrophilic and hydrophobic ends
fetal development → without surfactants, premature fetuses often experience alveolar collapse and are less likely to survive


Respiratory Volumes and Capacities
used to assess respiratory statues
tidal volume (TV) → normal in or normal out
inspiratory reserve volume (IRV) → normal in (EXTRA in)
if measure both inspiratory capacity ( = TV + RV)
Expiratory reserve volume (ERV) - Normal in. Normal Out. EXTRA OUT
Residual volume (RV) → amount you can’t get out
Vital capacity
total amount of exchangeable air
vital capacity = TV + IRV + ERV
Functional Residual Capacity
amount of air in lungs after normal breath out
ERV + RV
Total Lung Capacity
max amount of air that could be in the lungs
TV + IRV + ERV + RV

Dead Space
anatomical dead space
no contribution to gas exchange
air remaining in passageways (~150 ml)
alveolar dead space
nonfunctional alveoli due to collapse/obstruction
total dead space
sum of anatomical dead space + alveolar dead space

Factors Impacting Pulmonary Ventilation
Lung Compliance → stretchability of the lung and openness of alveoli
Low Compliance Causes:
scar tissue
high surface tension
High Compliance Causes
emphysema

Daily Questions - Respiratory System
Why does your nose run when its cold outside?
humid environment with really cold water bottle → water on outside of water bottle (warm air with lots of water gets closer to cold water bottle, air around water bottle becomes colder and can’t hold as much water, so it sticks to the water bottle)
nose → very warm in body and in really cold environment (short distance and large temperature difference)
nasal cavity moves from warmer environment to colder environment (large shift)
breathe in → put water into air and make warmer
exhale → warm air holds more water, but as it moves out the cavity, temperature declines, so some water vapor gets deposited onto walls of nose (lots of water = some runs out and doesn’t get absorbed quick enough)
Elephant Shrew Nose (Lung Nose) Selective Advantage?
longer nose = looses less water with each breath out
in desert = important to keep as much water as possible