Ziolo Lectures Flashcards
The hematocrit is a
rapid assessment of blood composition.It is the percent of the blood volume that is composed of RBCs (red blood cells).
Buffy coat is negligible when calculating
hematocrit
Arterioles+capillaries+venules=
microcirculation
Flow =
volume per unit time
F= ΔP/R
Resistance is roughly
1/radius^4
Blood viscosity can
alter
resistance and thereby flow.
Main function of valves –
isolate electrically atria from ventricle.
cardiac muscle isElectrically coupled through
gap junctions located in intercalated disc.
Parasympathetic releases ——— to
acetylcholine to muscarinic receptors
Sympathetic releases ——— to
norepinephrine/epinephrine, Beta = beta adronergic receptors.
Both nodes can
spontaneously depolarize – SA does this faster.
Bundle of His
depolarizes slower than AV node.
The rapid opening of voltage-gated sodium channels is responsible for
the rapid depolarization phase.
The prolonged “plateau” of
depolarization is due to the
slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channelsCalcium influx doesn’t allow for
repolarizing. Longer refractory period.
Opening of potassium
channels results in the
repolarization phase.
Sodium ions can “leak” in through
the
F-type [funny] channels
calcium ions
can move in through
the T [calcium] channels cause a
threshold graded depolarization.
The rapid opening of voltage-gated
calcium channels is responsible
for the
rapid depolarization phase
Reopening of potassium channels
PLUS
closing of calcium channels
are responsible for the
repolarization phase.
Excitation-Contraction Coupling links the
cardiac muscle cell action potentials
to contraction via control of calcium within the myocardium.
First heart sound –
closure of the AV valves
Second heart sound –
closure of the aortic and pulmonary valves
Murmurs
stenosis
Stenosis =
narrowing
Regurgitation =
insufficiency
Systole:
ventricles contracting
Diastole:
ventricles relaxed
Cardiac output (CO) =
Heart rate (HR) x Stroke volume (SV)
Atria influences
HR,
ventricles influence
stroke volume.
PS only decreases
HR.
To speed up the heart rate:
deliver the sympathetic hormone, epinephrine, and/or
release more sympathetic neurotransmitter (norepinephrine), and/or
reduce release of parasympathetic neurotransmitter (acetylcholine).
Preload –
the volume of blood in the ventricles just before contraction. End-diastolic volume
Afterload –
the pressure against which the ventricle pumps
To increase the heart’s stroke volume:
fill it more fully with blood. The increased stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap.
To further increase the stroke volume:
fill it more fully with blood AND
deliver
sympathetic signals (norepinephrine and epinephrine); it will also relax more rapidly, allowing more time to refill
Sympathetic signals (norepinephrine and epinephrine) cause a
stronger and more rapid contraction and a more rapid relaxation.
To increase SV, increase:
end-diastolic volume, norepinephrine delivery from sympathetic neurons, and epinephrine delivery from the adrenal medulla
To increase HR, increase:
norepinephrine delivery from sympathetic neurons, and epinephrine delivery from adrenal medulla (reduce parasympathetic).
Thermodilution Cardiac Output
is a
measurement of cardiac function
Ejection fraction =
measurement of contractility. Defined as the ratio of the stroke volume (end diastolic volume [EDV] minus end systolic volume [ESV]) to the end-diastolic volume
EDV-ESV/EDV.
Hypertrophic cardiomyopathy is
preload dependent
Arterioles can adjust
diameter to regulate blood flow.
In response to the pulsatile contraction of the heart:
pulses of pressure move throughout the vasculature, decreasing in
amplitude with distance
Compliance =
Δ volume/Δ pressure
Veins and venules have highest .
compliance
Maximum arterial pressure =
systolic pressure (SP)
Minimum arterial pressure =
diastolic pressure (DP)
Pulse pressure =
SP – DP
Pulse pressure isDetermined by:
stoke volume
Speed of ejection of the stroke volume
Arterial compliance
Mean arterial pressure =
DP + 1/3(SP-DP)
MAP =
pressure driving blood into the tissues
averaged over the cardiac cycle
Arterioles
Determine the relative blood flow to that organ
In composite determine the mean arterial pressure
Forgan=
(MAP- venous pressure)/Resistanceorgan
because venous pressure is close to) 0 mmHg
Forgan=
MAP/Resistanceorgan
Dynamic adjustments in the blood distribution to the
organs is accomplished by
relaxation and contraction
of circular smooth muscle in the arterioles.
Arteriole Intrinsic tone
Controlled by:
Local controls
Extrinsic controls
Active hyperemia and flow autoregulation differ in their
cause but both result
in the production of the same
local signals that provoke vasodilation.
Local controls (arteriole intrinsic tone)
Active hyperemia
Flow autoregulation
Active hyperemia:
** accumulation of: CO2, H+, K+, eicosanoids, adenosine, bradykinin, nitric oxide (NO)
Flow autoregulation:
- myogenic responses – some arteriolar smooth muscle respond to increased stretch caused by increased pressure by contracting to a greater extent (Converse is also true).
- Reactive hyperemia – response to cessation of blood flow
- myogenic responses – some arteriolar smooth muscle respond to increased stretch caused by increased pressure by contracting to a greater extent (Converse is also true).
Sympathetic stimulation of alpha-adrenergic receptors causes
vasoconstriction to decrease blood flow to that location.
Sympathetic stimulation of beta-adrenergic receptors leads to
vasodilation to cause an increase in blood flow to that location.
Endothelial controls: Arterioles:
Paracrine effect:
Flow induced arterial vasodilation
Paracrine effect:
Vasodilators: -Endothelium derived relaxing factor (EDRF) = Nitric oxide (NO) -Prostacyclin (PGI2) Vasoconstrictor -Endothelin-1
Diversity among signals that influence contraction/relaxation
in vascular circular smooth muscle implies a diversity of
receptors and transduction mechanisms.
Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream metarterioles and precapillary sphincters determine the
volume of blood each capillary receives
Low molecular weight penetrating solutes =
crytalloids
Non-penetrating plasma proteins =
colloids
PC=
capillary hydrostatic pressure (favoring fluid movement out of the capillary
PIF=
Interstitial hydrostatic pressure (favoring fluid movement into the capillary)
πC=
Osmotic force due to plasma protein concentration (favoring movement into the capillary)
πIF=
Osmotic force due to interstitial fluid protein concentration (favoring movement out of the capillary
At rest, approx.
60% of the total blood volume is in the veins.
Sympathetically mediated venoconstriction can substantially
increase venous return to the heart.
Alterations in “venous return” alter
end-diastolic volume (EDV);
increased EDV directly increases
stroke volume and cardiac output.
vFerritin serves as a storage buffer for
iron
RBC life span ~
120 days, 1% of RBC replaced daily (~250 billion RBC)
Iron released from destroyed RBC is bound by
transferrin and delivered to bone marrow.
Erythropoiesis is
hormonally regulated:
decreased oxygen delivery to the kidney causes the secretion of erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis.
Anemia: Decrease in the ability of the blood to
carry oxygen
due to:
- decrease in the total number of erythrocytes
- diminished concentation of hemoglobin
- combination
Collagen is a
“magnet for platelets,”
which then become one of the sources of signals that alter blood flow and initiate the steps of clot formation at the affected site
Thrombin IX loss results in
Genetic absence results in hemophilia
excessive bleeding
*Clotting can occur in the absence of all
cellular elements except
platelets***
Delta P, which is called the perfusion pressure, is the same for all
vascular beds; it is equal to MAP–VP, (VP is venous pressure)
Because blood flows along the path of
least resistance, organs with the lowest resistance will receive the highest flow.
Most of the decrease in resistance will be in the
arterioles. They have the most smooth muscle and they also have the largest resistance.
Mean systemic arterial pressure is the product of
cardiac output and total peripheral resistance (TPR)
TPR =
the sum of the resistances to flow offered by all the systemic blood vessels
MAP =
CO x TPR
all changes in mean arterial pressure must be the result of changes in
cardiac output and/or total peripheral resistance
Compensatory changes in arteriolar resistance occur to protect the
maintenance of mean arterial pressure
Systemic vascular system is a series of tube….therefore delta P =
mean systemic artereial pressure (MAP) – pressure in the right atrium.
**BUT: RAP ~O mmHg, so MAP = COXTPR
F = CO and R = TPR
MAP is the perfusion pressure for all
vascular beds and therefore very important.
Baroreceptor neurons function as sensors in the
homeostatic maintenance of MAP by constantly monitoring pressure in the aortic arch and carotid sinuses.
Baroreceptor neurons deliver MAP information to the
medulla oblongata’s cardiovascular control center (CVCC);
the CVCC determines autonomic output to the heart.
The information reported by
baroreceptor neurons sets in motion autonomic responses not only to the heart, but also to
arterioles and veins.
If arterial pressure decreases, the discharge rate of the
arterial baroreceptors decreases
Fewer impulses travel up the afferent nerves to the medullary cardiovascular center and this induces:
(When arterial baroreceptor discharge rate drops)
increased HR because of increased sympathetic activity to the heart and decreased parasympathetic activity
2) increased ventricular contractility because of increased sympathetic activity to the ventricular myocardium
3) arteriolar constriction because of increased sympathetic activity to the arterioles
4) increased venous constriction because of increased sympathetic activity to the veins
- ↑CO (↑ HR ↑ SV) ↑ TPVR normalization of BP
Sorry about text vomit, know that the reciprocal can occur.
an abnormal increase in MAP “squeezes” more fluid out of the blood and into the
urine, leading to a reduction in blood volume, which then reduces MAP back closer to the “set point” value.
At capillaries, reduced MAP increases
absorption and
reduces filtration to help “protect” blood volume.
Hypotension - Allergic response
Histamine release –> vasodilation
Hypotension: Emotional stress
↓Sympathetic and ↑Parasympathetic
-vasovagal syncope
Pressure at a given point =
cardiac generate pressure + pressure equal to the weight of the column of blood to the point measured.
Decrease in total peripheral resistance is seen during
exercise
Increase in CO during exercise
is due to large increase in
HR and
smaller increase in SV (stroke volume)
VO2max could be limited by:
1- cardiac output
2- respiratory system’s ability to deliver oxygen
3- exercising muscle’s ability to use oxygen
Except for highly trained athletes –
CO is the factor that
determines VO2max
Renal hypertension –>
increased renin release –>
increased angiotension II release
Diastolic dysfunction – reduced
ventricular compliance results in an
increase end-diastolic pressure and thus a decreased end-diastolic
volume and a decreased stroke volume.
Systolic dysfunction – a decrease in
cardiac contractility – a lower
Stroke volume at any given end-diastolic volume.
To further increase the stroke volume:
fill it more fully with blood
AND
deliver sympathetic signals (norepinephrine and epinephrine);
it will also relax more rapidly, allowing more time to refill
Heart failure leads to increased fluid retention, leading to
increased blood volume and greater stroke volume;
however, the failing heart is less able to handle a
large EDV.
Sudden cardiac death occurs from
ventricular fibrillation.
Thrombolytic therapy
Streptokinase
tissue plasminogen activator
Percutaneous coronary intervention
Balloon angioplasty
Stenting
Stroke volume is regulated through changes in:
the END-DIASTOLIC VOLUME (the PRELOAD): the size of the heart just before it contracts
2. cardiac CONTRACTILITY (the amount of free Ca2+ in ventricular muscle cells)
The EDV is the volume of the ventricle when it is
completely filled, just before it contracts.
sorry, I’m dumb and keep mixing this up
larger EDV (PRELOAD) produces a
STRONGER contraction and a LARGER SV
Frank sterling mech
The length-tension relationship of cardiac muscle is responsible for the
Frank-Starling mechanism
larger EDV leads to a larger
initial fiber length
F-s relationship MATCHES the
CO to the VENOUS RETURN
F-s relationship it matches the outputs of the
two VENTRICLES
Sympathetic response increases stroke volume by increasing
calcium
