Exam 3 Flashcards
cardiac muscle
both extracellular and intracellular ca2+ like skeletal muscle
need ATP to pump ca2+ back out (low conc->high conc
T-tubule structure is diff
ca2+ more extracellular, so moves in via L-type ca2+ channels
longer refractory period (no tetnus)
pacemaker potential is 60 mV (Na+ in via If channels; does not depend on ca2+ so AP is all or nothing)
3 basic components of cardiovascular system
heart=pump
blood vessles=tubes
blood=fluid
SA node
regulation of HR
intercalated disks w/ gap junctions
transmits electrical and chemical signals and generates force
order of electrical signal
SA node->AV node->AV bundle->purkinje fibers
p wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
R
signal goes to purkinje fibers and depolarizagion occurs
EKG
helps determine if there are abnormal signals in the heart
third degree block
no T waves
A-fib
no P or T waves
ventricular fibrilation
no normal waves
chordinae tendinae
anchor valves and help them open and close
high to low BP
aorta
arteries
aterioles
capillaries
venules
veins
vena cava
smaller radius
higher resistance
less flow
larger radius
less resistance
higher flow
systole
contraction
diastole
relaxation
more narrow vessle
faster velocity of flow
frank-starling law
can accomodate stretch and generate force (exercise)
heart failure with preserved ejection fraction
diastolic dysfunction
EF>50%
hypertension, lung congestion, exercise intolerance, muscle weakness, A-fib, renal dysfunction
SGLT2 (antidiabetic= reduced glucose levels)
hypertrophy
building up muscle
precapilary spincter
close off to prevent BF
valves
prevent backflow of blood in veins
skeletal muscle pump
when skeletal muscles compress in veins they force blood towards the heart
pulse pressure
systolic pressure-diastolic pressure
MAP
diastolic pressure + 1/3 (pulse pressure)
proportional to CO and resistance
increased resistance
increased MAP
decreased CO
decreased BV and MAP
CO
HR * SV
decreased venous BV
increased arterial BV
increase in BP fast response
vascodilation
decreased CO
decreased BP
increase in BP slow response
excretion of fluid in urine via kidneys
decreased BV
hemorrhage
decreased BV and decreased BP
so vasoconstriction= increased CO, increased HR (sympathetic response)
SV
EDV-SDV
arteriole resistance modulation
local control match tissue metabolic needs
sympathetic reflexes
hormonal control (vasopression and angiotensin II)->vasocontriction
epinepherine, decreased O2, increased Co2, increased H+ and K+-> vasodilation
hyperemia
increased BF to a region
inflammation
increased temp
tonic control
increased NE (vasocontriction)
decreased NE (vasodilation)
parallel arrangement
allows to sense changes
affect BF to diff parts of body
baroreceptors
located in carotid and aortic arteries
increased BP-> decreased sympathetic response-> increased parasympathetic response-> vasodilation-> decreased CO, R, HR-> decreased BP
contain stretch sensitive ion channels (mechanically gated)
depolarization due to Na+ and ca2+
orthostatic hypotension
change in position due to standing lowers BP
due to gravity causing accumulation of blood in the venous cavity (no venous return)-> decreased CO and MAP
standing activates skeletal muscle pump increasing BP
low gravity causes more blood in arterial circulation (increased BV and BP)-> decreased BV via kidneys (dehydration)
capillaries
high SA but low BF
O2 (via diffusion)
paracellular route (H2O)
transcytosis (macromolecules)
fenestrated
specialized pores
colloid osmotic pressure
amount of protein present mediated capillary exchange
decreased hydrostatic pressure
absorption
increased hydrostatic pressure
filtration
kwashiorkor
malnutrition
increased net filtration (of fluid but little nutrients)
fluid buildup in extracullar fluid
decreased colloid osmotic pressure (decreased protein= watery plasma)
order of cardiac cycle
late diastole
atrial systole
isovolumetric contraction
ventricular ejection
isovolumic ventricular relaxation
respiratory system
exchange of o2 and co2 b/w lungs and blood
transport of o2 and co2 by the blood
exchange of gases b/w blood and cells
consist of an increased SA
alveoli
form exchange system in lungs
type 1= gas exchange
type 2= surfactant (help airsacs stay open)
bronchioles
help get air into lungs
cillia
help move debris away from lungs
secrete saline
goblet cells
secrete mucous
CFTR
help move mucous
impaired in patients w/ CF
dead space
air that is not exchanged in alveoli
functions of airways
exchange of gases
pH, water, and heat regulation (loss)
protection from pathogens
vocalization
movement of air (resistance and muscular pump)
importance of pleural fluids and membranes
reduce friction
position
elastic recoil and movement of lungs
pneumothorax
collapsed lung
increased BV
increased filtration
fluid accumulation in lungs
symptoms of CHF
edema and fluid buildup in lungs
boyle’s law
decreased volume= increased pressure (exhalation)
increased volume during inhalation= decreased pressure (diaphram flattens)
muscle groups= internal (expiration) and external (inhalation) intercostals
compliance
ability of lungs to stretch
elastance
ability to resist being deformed
emphysema
lungs are able to stretch, but lack elastic recoil
surfactant
prevent adhesion
decrease surface tension
bronchodilators
epinepherine (B2 receptors)
good for asthma attacks
hyperventilation
pp of increased o2
pp of decreased co2-> decreased H+-> increased pH
increased alveolar ventilation
minimal increase in percent saturation of aterial Hb
physiological sensors
o2
co2
pH
decreased pp of o2
decreased o2 in alveoli
can be due to altitude, edema, emphysema, asthma, CNS depression (can lead to hypoxia)
hypercapnia
high co2 levels
solubility
co2 more soluble than o2
o2 bound to hemoglobin helps increase solubility (3 diff cells o2 has to pass)
hemoglobin
4 chains (2 alpha and 2 beta)-> heterotetramer
4 heme groups
cooperativity of binding= interaction of o2 w/ one heme faciliates binding of o2 to another heme
pulse oximeter
measures hemoglobin saturation
hypoxic hypoxia
low arterial pp of o2 (high altitude, alveolar hypoventilation, decreased lung diffusion capacity)
anemic hypoxia
decreased total amount of o2 bound to hemoglobin (blood loss, CO poisoning)
ischemic hypoxia
reduced BF (HF, shock, thrombosis)
pp of o2 of venous blood
equal of pp of o2 of muscle
CO2
7% dissolved in blood
23% binds to Hb (decreased Hb affinity for o2)
70% converted to HCO3 (binds to carbonic anahydrase)-> converted to CO2+H2O-> acts as a buffer-> dissociation of H+ decreased pH
reflex control of ventilation
controlled of respiratory neurons in medulla
neurons in pons interacts w/ medullary neurons to influence ventilation
modulated by chemoreceptors and mechanoreceptors linked receptors
cardiac muscle characteristics
striated
sarcomeres
heart muscle
uninucleate
intermediate
graded
autorhythmic
autonomic neurons
epinepherine
