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456 Cards in this Set
- Front
- Back
what is produced by myoendocrine cells of the heart?
|
atrial natriuretic factor (ANF)
|
|
in what layer of the heart are myoendocrine cells found?
|
myocardium
|
|
where is the tricuspid valve?
|
aka right AV valve
between the right atrium and the right ventricle |
|
where is the bicuspid valve?
|
aka left AV valve
between the left atrium and the left ventricle |
|
what is caused by a rupture of the chordae tendinae?
|
prolapse of the cusps of the valve
|
|
what are the two semilunar valves?
|
aortic and pulmonic valves
|
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what is meant by the term "peripheral circulation"?
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all circulation outside of the coronary circulation
|
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what is meant by the term "systemic circulation"?
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all circulation supplied by the aorta and its branches
|
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what are the functions of the circulation?
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provide oxygen and nutrients to body tissue
remove waste products from body tissue temperature regulation |
|
what is the site of the highest resistance in the cardiovascular system?
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arterioles
small arteries and arterioles account for 70% of the pressure drop in the circulation |
|
what are alpha1 receptors?
|
adrenergic receptors on the arterioles of skin, splanchnic and renal circulations, as well as veins
|
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what are beta2 receptors?
|
adrenergic receptors on the arterioles of skeletal muscle
|
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what makes up the largest total cross-sectional and surface area of all types of blood vessels?
|
capillaries
|
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what type of adrenergic receptors do veins have that decrease their compliance?
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alpha1 adrenergic receptors
|
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what is the pulmonary capillary wedge pressure used to estimate?
|
left atrial pressure
|
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what is a normal pulmonary capillary wedge pressure?
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8-10 mmHg
|
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at what pulmonary capillary wedge pressure does a person have pulmonary edema?
|
greater than 20 mmHg
|
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when can pulmonary capillary wedge pressure be increased?
|
hypervolemia
left ventricular failure |
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when can pulmonary capillary wedge pressure be decreased?
|
hypovolemia
right ventricular failure |
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what is systolic failure of the left ventricle?
|
inability of the left ventricle to contract
|
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what is diastolic left ventricular failure?
|
inability of the left ventricle to relax
caused by stiffness |
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what is caused by left ventricular failure?
|
increased left atrial presure
backup of blood in the lungs pulmonary edema |
|
what are the symptoms of left ventricular failure?
|
dyspnea on exertion
orthopnea paroxysmal nocturnal dyspnea fatigue, eventually confusion |
|
what are the signs of left ventricular failure?
|
S3 gallop, S4
lung crackles dullness to percussion of chest |
|
what is caused by right ventricular failure?
|
increased venous pressure
backup of blood in leg veins peripheral edema |
|
what is ascites?
|
excess fluid in the space between the tissues lining the abdomen and abdominal organs (the peritoneal cavity)
|
|
what are the symptoms of right ventricular failure?
|
ascites (fluid in the abdominal cavity)
shortness of breath (due to mechanical impingement of diaphragm) jugular venous distention nocturia (night time urination caused by increased venous return with leg elevation) |
|
what is orthopnea?
|
dyspnea when lying down
|
|
what is dyspnea?
|
shortness of breath
|
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what is a main difference between the symptoms of left vs. right ventricular failure?
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left ventricular failure symptoms change on lying down, while right ventricular failure symptoms do not
|
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what is unstressed volume in cardiovascular circulation?
|
blood volume in veins
|
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what is stressed volume in cardiovascular circulation?
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blood volume in arteries
|
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how much blood volume is in the heart at any given time? (not including coronary arteries)
|
8-11%
|
|
how much blood volume is in the lungs at any given time?
|
10-12%
|
|
how much blood volume is in the systemic arteries at any given time?
|
10-12%
|
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how much blood is found in systemic veins at any given time?
|
60-68%
(mostly in small veins and venules) |
|
how much blood volume is found in capillaries at any given time?
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4-5%
|
|
what is the formula for velocity of blood flow?
|
v = Q / A
|
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what formula relates cardiac output, pressure and resistance?
|
Q = dP / R
CO = (MAP - RAP) / TPR |
|
what is the formula for organ resistance?
|
R = (PA - PV) / CO
R - organ resistance PA - pressure in the organ's artery PV - pressure in the organ's vein CO - cardiac output |
|
what is Poiseuille's Law?
|
R = (8etaL) / (pi r^4)
R - resistance of vessel eta - viscosity of fluid L - length of vessel r - radius of vessel |
|
what are the important points to take away from Poiseuille's Law?
|
resistance is directly proportional to viscosity of fluid and length of vessel
resistance is indirectly proportional to radius raised to the fourth power |
|
what are the assumptions that make Poiseuille's Law true?
|
1 - steady, non-pulsatile, flow
2 - uniform flow (long vessel with constant cross-section) 3 - newtonian fluid (constant viscosity) 4 - laminar flow 5 - no-slip condition (velocity near wall is very low) |
|
what is the formula for conductance?
|
C = 1 / R
|
|
what is the viscosity of plasma?
|
about 1.5 times viscosity of water
|
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what is the viscosity of blood?
|
normal - about three times viscosity of water
high hematocrit - up to ten times viscosity of water low hematocrit (anemia) - about 1.5 times viscosity of water - close to plasma viscosity |
|
why are stenoses so dangerous when they're found?
|
generally not symptomatic (flow does not significantly drop off) until stenosis has reaches around 85% area reduction
|
|
what is laminar flow?
|
non-turbulent flow, which occurs in layers, along streamlines
characterized by a reynold's number less than 2000 |
|
what is transitional flow?
|
flow which is not laminar but isn't turbulent
characterized by a reynold's number between 2000 and 3000 |
|
what is turbulent flow?
|
random three-dimensional fluid motion superimposed on the average motion
characterized by a reynold's number above 3000 |
|
what is a reynold's number?
|
a dimensionless number which acts as a measure of the turbulence of fluid flow
|
|
where is turbulence normally found in normal humans?
|
aorta
carotid sinus |
|
what are murmurs?
|
blowing, gurgling, whooshing, or rasping sounds produced by turbulent blood flow through the heart valves or near the heart
|
|
what is a bruit?
|
the sound of blood flowing through a narrowed portion of an artery
|
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what is the formula for the compliance of a blood volume?
|
C = dV / dP
|
|
what is the significance of compliance?
|
the higher the compliance, the smaller the pressure change for a given change in volume
the higher the compliance, the more volume the vessel can hold |
|
in what generalized ways can central venous pressure be changed?
|
increased blood volume
increased contraction of smooth muscles in the veins (decreased compliance) |
|
how does compliance vary with age?
|
increases in children, adolescents, and young adults
reaches a plateau near age 30 declines beyond 30 years (even in those free of cardiovascular disease and risk factors) |
|
what are the three important parts of the pulsatile arterial pressure?
|
ascending limb (anacrotic limb)
descending limb (catacrotic limb) incisura (dichrotic notch) |
|
what causes the ascending limb in arterial pressure?
|
rapid rise in pressure during ventricular systole
|
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what causes the descending limb of arterial pressure?
|
fall in pressure during diastole
|
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what causes the dichrotic notch in arterial pressure?
|
closing of aortic valve at the end of ejection, causing a brief retrograde flow
|
|
what blood pressure constitutes hypertension?
|
systolic consistently over 140mmHg and/or diastolic consistently over 90mmHg
|
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on what is systolic pressure mainly dependent?
|
stroke volume
compliance |
|
on what is diastolic pressure mainly dependent?
|
heart rate
arteriolar resistance |
|
why is diastolic pressure low in athletes?
|
low heart rate, allowing more time for pressure to drop off between fillings
|
|
what is pulse pressure?
|
PP = SP - DP
PP - pulse pressure SP - systolic pressure DP - diastolic pressure |
|
what happens to pulse pressure in patients with essential hypertension (primary hypertension)?
|
moderate increase in diastolic pressure
substantial increase in systolic pressure pulse pressure increased |
|
what happens to pulse pressure in patients with severe arteriosclerosis?
|
ventricular ejection
increase in capillary flow during systole nearly no capillary flow during diastole large pulse pressure |
|
what happens to pulse pressure in patients with chronic aortic valve regurgitation?
|
SV is increased to compensate for backleaking during diastole
pulse pressure increased |
|
what happens to the pulse pressure in well-trained athletes?
|
low resting heart rate leads to prolonged ventricular filling times and high SV
pulse pressure increased |
|
how do you calculate mean arterial pressure (MAP)?
|
MAP = (2DP + SP) / 3
DP - diastolic pressure SP - systolic pressure |
|
what is central venous pressure?
|
pressure of the thoracic vena cava near the right atrium
right atrial pressure (2-6mmHg) filling pressure preload |
|
what is automaticity?
|
the ability to excite spontaneously
|
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what is rhythmicity?
|
the regularity of the heart beat
|
|
what is conductivity?
|
the ability to conduct action potentials
|
|
what are the responsibilities of the SA node versus the AV node?
|
SA - heart rate
AV - conduction velocity |
|
what is phase 0 of the fast response cardiac action potential?
what ion movements are responsible? |
upstroke/depolarization phase
Na influx through V-gated Na channels |
|
what is the threshold for opening V-gated Na channels in the heart?
|
-65 mV
|
|
what are the two gates of a V-gated Na channel?
|
activation gate (m-gate)
inactivation gate (h-gate) "hi ma" |
|
how do the V-gated Na channels of the heart respond to tetrodotoxin?
|
they are mainly resistant, so they ignore it completely
|
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how does the response of the cardiac action potential change based on the resting membrane potential?
|
depolarizes more quickly, the more depolarized the membrane is
hyperpolarization increases dV/dT (more polarized cells have faster upstroke) depolarization decreases dV/dT (less polarized cells have a slower upstroke) |
|
what effect does moderate hyperkalemia have on the upstroke of a cardiac action potential?
|
depolarizes cell membrane (-90mV to -60mV)
inactivation gates of Na channels are closed smaller inward current (low dV/dT) (slow upstroke) |
|
what effect does mild hyperkalemia have on the upstroke of the cardiac action potential?
|
depolarization of cell membrane (-90mV to -80mV)
resting membrane potential closer to threshold potential fast upstroke (increase of dV/dT) |
|
what is Phase 1 of the fast response cardiac action potential?
what ions are responsible for it? |
initial repolarization (the spike)
fast Na channels close K flows out through channels creating Ito (transient outward current) |
|
what is Phase 2 of the fast response cardiac action potential?
what ions are responsible for it? |
plateau phase
K flows out through Kr and Ks channels Ca flows in (slowly) through mostly L-type channels |
|
what are Kr, Ks and K1 channels?
|
Kr - rapid rectifier
Ks - slow rectifier K1 - potassium leak channels |
|
what drugs block L-type Ca channels?
what is the effect? |
verapamil
nifedipine diltiazem no plateau phase (phase 2) in fast response cardiac AP |
|
why does the fast response cardiac AP have a plateau phase?
|
current of calcium out is approximately equal to current of potassium in (from both Kr and Ks channels)
ICa = IKr + IKs |
|
how does extracellular calcium affect contractility (strength of contraction) of the heart?
|
the calcium influx is involved in excitation-contraction coupling
higher extracellular calcium causes higher influx of calcium, leading to a stronger contraction |
|
what is phase 3 of the fast response cardiac action potential?
what ions are responsible for this phase? |
repolarization
calcium influx stops (slow channels close) K flows out through Kr and K1 channels |
|
what is phase 4 of the fast response cardiac action potential?
what ions are responsible for this phase? |
resting membrane potential
Na is exchanged for K through Na-K ATPase Na is exchanged for Ca through Na-Ca exchanger Ca is removed by Ca ATPase K leaks out at very low rate through K1 channels |
|
what is the effective refractory period?
|
time in which normally no AP occurs
includes absolute refractory period and then a little more |
|
what is the supranormal period?
|
time during which a slightly smaller than normal stimulus elicits a propagated response
these APs typically have a lower amplitude |
|
how does heart beat frequency increase?
|
shortens duration of AP, but not the refractory period
|
|
why is it important to have a long refractory period in the heart?
|
want to have time to pump all blood out and then refill with some blood
|
|
what is the slow response cardiac action potential?
|
potential through the SA and AV nodes
|
|
what is the fast response cardiac action potential?
|
potential through atrial and ventricular myocytes
|
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what phases are missing in the slow response cardiac action potential (compared to the fast response)?
|
phase 1 (initial repolarization)
phase 2 (plateau) |
|
what is phase 0 of the slow response cardiac action potential?
what ions are responsible for this phase? |
depolarization
Ca flows inward through T-type channels |
|
what is phase 3 of the slow response cardiac action potential?
what ions are responsible for this phase? |
repolarization
K flows out |
|
what is phase 4 of the slow response cardiac action potential?
what ions are responsible for this phase? |
spontaneous diastolic depolarization
Ir (funny current) - Na influx causing depolarization ICa - Ca influx causing depolarization IK - K outflow opposes Ir and ICa - diminishes as phase 4 progresses |
|
what is Ir?
|
aka funny current
the inward flow of Na during phase 4 of the slow response cardiac AP it is through channels different from the fase Na channels, which are activated at or below -50mV |
|
when do the different channels open/close in phase 4 of the slow response cardiac AP?
|
Na "funny channels": open at or below -50mV
Ca channels: open at -55mV K channels: progressively close throughout phase 4 |
|
what are the normal pacemaker cells? what other cells can takeover as abnormal (latent) pacemaker cells?
|
normal - SA node cells
abnormal - AV node cells, bundle of His, Purkinje fibers |
|
how do SA node cells suppress the automaticity of other cells?
|
SA node cells stimulate the other cells at a frequency higher than their intrinsic rhythm; if the SA node fails, the site with the next highest frequency will take over, etc.
|
|
what happens to the autorhythmicity in a complete heart block?
|
in a complete heart block, the AV node no longer sends action potentials from atria to ventricles
SA node sets the frequency for the atria and Purkinje fibers set the frequency for the ventricles this causes atrial fibrillation |
|
what happens to the autorhythmicity in a premature beat (PVC)?
|
an ectopic pacemaker (e.g. the purkinje fibers) gets a much higher intrinsic frequency than the SA node and it begins to control the heart rate
whole heart beats more rapidly |
|
from where do the preganglionic parasympathetic nerves for the heart originate?
|
dorsal motor nucleus of the vagus
nucleus ambiguus (medulla oblongata) |
|
what are the efferent nerves of the parasympathetic innervation of the heart?
|
vagus nerves
|
|
what are the effector organs of the parasympathetic innervation of the heart?
|
SA node
AV node few blood vessels |
|
what are the effector organs of the sympathetic innervation of the heart?
|
SA node
AV node atrial myocardial cells ventricular myocardial cells blood vessels |
|
where are the postganglionic cells located for the parasympathetic and sympathetic innervation of the heart?
|
parasympathetic - at epicardial surface or within the walls of the heart near SA and AV node
sympathetic - in stellate and middle cervical ganglia |
|
in what efferent nerves is the sympathetic innervation of the heart carried?
|
paravertebral chains from thoracic sympathetic chain ganglia
|
|
from where do the preganglionic sympathetic neurons of the heart originate?
|
spinal cord (C7,C8, T1-T6)
|
|
what are the control centers for the autonomic innervation of the heart?
|
hypothalamus, thalamus, cerebral cortex - response to environmental or emotional triggers
medulla oblongata PS - nucleus vagus & ambiguus; triggered by reflexes and respiratory center S - rostral ventrolateral nucleus; distinct accelerator and augmentor cells; provide tonic excitatory activity to heart and blood vessels |
|
what are chronotropic effects?
|
those that change the heart rate
|
|
what are dromotropic effects?
|
those that change the conduction velocity of the AV node and subsequently the rate of electrical impulses in the heart
|
|
through what receptors does parasympathetic innervation affect the heart?
|
muscarinic acetylcholine receptors (M2 type)
|
|
what is blocked by atropine?
|
muscarinic acetylcholine receptors
|
|
what are inotropic effects?
|
those that alter the force or energy of muscular contractions
|
|
why can the parasympathetic system exhibit beat by beat control over the heart?
|
the effects appear and disappear very quickly due to high efficiency of acetylcholinesterase
|
|
how does the parasympathetic system cause a negative chronotropic change?
|
muscarinic ACh receptors open potassium channels, increasing the permeability of K
they also decrease the permeability of Na |
|
how does the parasympathetic system exhibit a negative dromotropic effect?
|
decreases Ca influx
increases K outflow |
|
through what receptors does the sympathetic system affect the heart?
|
beta1-adrenergic receptors
|
|
what is isoproterenol?
|
beta1-receptor agonist
(increases sympathetic effects on the heart) |
|
what are beta blockers?
|
beta1-receptor antagonists (e.g. propanolol)
(decreases sympathetic effects on the heart) |
|
how does the parasympathetic system have its minor inotropic effect?
|
some parasympathetic neurons terminate on sympathetic neurons, inhibiting them
|
|
how does the sympathetic system exhibit positive chronotropic effects?
|
increases Na permeability
|
|
how does the sympathetic system exhibit positive dromotropic effects?
|
increases calcium influx
|
|
how does the sympathetic system exhibit positive inotropic effects?
|
increases calcium influx
|
|
what are the neurotransmitters used by the parasympathetic system?
|
preganglionic - ACh
postganglionic - ACh |
|
what are the neurotransmitters used by the sympathetic system?
|
preganglionic - ACh
postganglionic - NE |
|
what is respiratory sinus arrhythmia?
|
subtle, naturally occuring arrhythmia that occurs through the influence of breathing on the sinoatrial node.
mainly controlled by PS, since it is responsible for beat-to-beat control, but S does contribute |
|
how is the heart rate affected by inhalation?
|
decreased thoracic pressure
PS is inhibited heart rate increases |
|
how is the heart rate affected by exhalation?
|
increased intrathoracic pressure
PS active heart rate decreases |
|
what does the respiratory sinus arrhythmia indicate to a clinician?
|
if there is no RSA, it indicates that there is inefficient ANS control and the person is in grave danger
|
|
what is contractility?
|
change in contractile force independent of initial fiber length
cardiac performance at a given preload, afterload, and heart rate |
|
what is afterload?
|
equivalent to TPR, afterload is what the heart must push against to get blood out of it
|
|
what is preload?
|
equivalent to the volume of blood in the aorta/ventricle, preload is what the heart must overcome before it contracts
|
|
how does the parasympathetic system affect a Frank-Starling Curve?
|
moves it down and right
|
|
how does the sympathetic system affect a Frank-Starling Curve?
|
moves it up and left
|
|
what factors can increase heart contractility?
|
caffeine
catecholamines thyroxin insulin digitalis |
|
what factors can decrease heart contractility?
|
severe hypoxia
severe hypercapnea low pH |
|
what is hypercapnea?
|
excess CO2 in the blood
|
|
which electrode is the recording electrode?
|
positive electrode
(i.e. the camera taking the picture) |
|
what happens in an ECG when the depolarization travels toward the positive electrode?
|
upright wave
|
|
what factors affect the magnitude of a wave in an ECG?
|
amplitude of depolarization vector
angle of depolarization vector compared to the lead |
|
what happens in an ECG when the depolarization vector travels away from the positive electrode?
|
inverted wave
|
|
scalar vs. vector ECG
|
scalar is normal type, plotting voltage vs. time
vector ECG shows resultant vector moving in 3D and providing info. on angle and magnitude |
|
what is an Einthoven triangle?
|
imaginary equilateral triangle with the heart at the center and formed by lines that represent the three standard limb leads of the ECG
|
|
by convention, what point represents the groin in the Einthoven triangle?
|
left leg
|
|
what are the 6 frontal plane leads?
|
standard bipolar limb leads (I, II, and III)
augmented unipolar leads (aVR, aVL, aVF) |
|
what is lead I?
|
right arm negative
left arm positive from right arm to left arm |
|
what is lead II?
|
right arm negative
left leg positive from right arm to left leg |
|
what is lead III?
|
left arm negative
left leg positive from left arm to left leg |
|
what is aVR?
|
left arm + left leg = negative
right arm = positive from abdomen to right arm |
|
what is aVL?
|
left leg and right arm = negative
left arm = positive from abdomen to left arm |
|
what is aVF?
|
right arm + left arm = negative
left leg = positive from abdomen to left leg |
|
what are precordial leads?
|
V1, V2, V3, V4, V5, V6
unipolar leads which view the electrical activity of the heart in the horizontal plane |
|
what is used as the negative electrode for the precordial leads?
|
Wilson's central terminal
|
|
what are the important landmarks for the placement of the precordial leads of an EKG?
|
V1-V3 in fourth intercostal space
V1 is right of sternum V2 is left of sternum V4-V6 in fifth intercostal space V4 is in left midclavicular line V6 is in left midaxillary line |
|
what are the inferior leads of a 12 lead EKG?
from what vantage point are they looking? |
II, III, aVF
diaphragmatic wall of the left side |
|
what are the lateral leads of a 12 lead EKG?
from what vantage point are they looking? |
I, aVL, V5, V6
lateral wall of the left side |
|
what are the septal leads of a 12 lead EKG?
from what vantage point are they looking? |
V1, V2
septal wall of the left ventricle |
|
what are the anterior leads of a 12 lead EKG?
from what vantage point are they looking? |
V3, V4
anterior wall of the left ventricle |
|
what is the simplified version of what you can see with what leads?
|
Lead I - lateral view - left atrium & ventricle
Lead II - inferior view - left and right ventricles Lead III - inferior view - right and left ventricles |
|
what is happening in the P wave?
|
atrial depolarization (movement of depolarization from SA node to AV node
upright in II, III, aVF inverted in aVR ***must be upright in II and aVF and inverted in aVR to designate a sinus rhythm*** |
|
what is happening during the PR interval?
|
atrial depolarization
delay of depolarization in the AV junction (allowing time for atria to contract before ventricles) depolarization of Bundle of His depolarization of bundle branches depolarization of Purkinje fibers |
|
what is the difference between the PR interval and the PR segment?
|
PR interval includes P wave, whereas PR segment does not
|
|
what is happening during the QRS waves?
|
ventricular depolarization
|
|
what is the definition of a Q wave?
what causes a normal Q wave? |
initial negative deflection from the baseline
***if there is no negative deflection, there is no Q wave*** septal depolarization in a left to right direction |
|
where can a Q wave be recorded?
|
leads with positive electrodes on the left side of the body (I, aVL, V6)
|
|
what is the R wave?
what causes it? |
R wave is a positive deflection from the baseline
normal depolarization of the ventricular wall which proceeds from endocardium to myocardium |
|
what is indicated by a larger R wave?
|
ventricular hypertrophy
|
|
what is indicated by a small R wave?
|
ventricular muscle damage
|
|
what is an S wave?
|
negative deflection that follows an R wave
|
|
what is an ST segment?
what is occurring in an ST segment? |
connects QRS complex to the beginning of the T wave
ventricles are all depolarized; the body is isoelectric |
|
what is the R wave?
what causes it? |
R wave is a positive deflection from the baseline
normal depolarization of the ventricular wall which proceeds from endocardium to myocardium |
|
what is indicated by a larger R wave?
|
ventricular hypertrophy
|
|
what is indicated by a small R wave?
|
ventricular muscle damage
|
|
what is an S wave?
|
negative deflection that follows an R wave
|
|
what is an ST segment?
what is occurring in an ST segment? |
connects QRS complex to the beginning of the T wave
ventricles are all depolarized; the body is isoelectric |
|
what is the difference between ST segment and ST interval?
|
ST interval includes the T wave, whereas the ST segment does not
|
|
what occurs to cause the T wave?
|
ventricular repolarization
begins at the apex of the heart and proceeds superiorly |
|
when is the absolute refractory period in an EKG?
|
beginning of QRS complex - apex of T wave
|
|
when is the relative refractory period in an EKG?
|
from peak of T wave to the end of the T wave
|
|
what is the QT interval?
what is corrected QT interval? |
from beginning of Q wave to end of T wave
QT interval divided by the square root of the RR interval (corrects it for the heart rate) |
|
what is the U wave?
what causes a U wave? |
a small upright wave following the T wave, which isn't always seen
caused by repolarization of papillary muscles or Purkinje fibers |
|
in what condition is the U wave prominent?
|
hypokalemia
|
|
how much time is accounted for in one small horizontal box on an ECG paper? in one large box?
how much potential is represented by one large vertical box? |
0.04 sec
0.20 sec 0.5 mV |
|
what is a simple calculation for the heart rate?
|
HR = 300 / # of large boxes between beats
|
|
what is considered tachycardia?
normal heart rate? bradycardia? |
>150 bpm
60-100 bpm <50 bpm |
|
what is a normal sinus rhythm?
|
regular
every p followed by QRS every QRS followed by p every PR interval the same every PR interval <1 box p's are upright in lead II |
|
what is the mean electrical axis?
|
temporally summated vector over the entire process of ventricular depolarization
|
|
how does the mean electrical axis deviate in the hypertrophy of one ventricle?
|
deviates toward the hypertrophied ventricle
|
|
how does the mean electrical axis deviate in a bundle branch block?
|
deviates toward the blocked side
|
|
how is the mean electrical axis determined in the graphical method?
|
use any two of the frontal ECG leads
measure the height above and below the baseline subtract height below from height above drop perpendicular line from lead each lead at the right number draw a line from the origin through the intersection of the two lines |
|
what is an isoelectric lead?
|
a lead with equal R and S waves in opposite directions
it is approximately perpendicular to the Mean Electrical Axis |
|
how can one determine the mean electrical axis by estimation?
|
determine the isoelectric lead
estimate MEA as being perpendicular to that lead ID the lead that has the tallest R waves (this will be the closes vector to the MEA) |
|
how can a P wave be abnormal?
|
disappears
abnormal shape dissociation from QRS complex changing from up to down or down to up on the same lead |
|
how long is an abnormally long PR interval?
what does this abnormality indicate? |
>0.20 sec (one large or five small boxes)
indicates that impulses move through the AV node more slowly than normal |
|
how can the QRS complex be abnormal?
what do these abnormalities indicate? |
taller peak - hypertrophy of ventricles
shorter peak - cardiac myopathy, diminished muscle mass, fluid in pericardium, pulmonary emphysema wider - doesn't originate from AV node or above - bundle branch block, hypertrophy, hyperkalemia bizarre shape - block, scar, ventricular ectopic pacemaker |
|
what does an inverted, wide QRS complex indicate?
|
premature venticular contraction, with ectopic pacemaker in ventricle
|
|
what is an abnormality in the QT interval?
what does this indicate? |
prominent Q wave - past MI
prominent Q wave is wider than one small square or >1/4 the height of the R wave |
|
what is an abnormality in the ST segment?
what does this indicate? |
flat, downsloping, or depressed ST segments - coronary ischemia
elevation - myocardial infarction depression - ischemia |
|
what is the shape of a normal ST segment?
|
slight upward concavity
|
|
what is an abnormality of a T wave?
what does this indicate? |
inverted - bundle block, ischemia, digitalis toxicity
***T wave is normally inverted in aVR*** tall, peaked - hyperkalemia |
|
what are EKG symptoms of hyperkalemia?
|
tall, peaked T waves
wide, flat, or absent P waves prolonged PR intervals ST segment depression widened QRS complexes |
|
what happens to the QT interval with low blood calcium?
|
prolongation of QT interval
|
|
what does sinus bradycardia look like on ECG?
|
<60 bpm with every p followed by QRS, and every QRS followed by p
impulses originate at SA node at slow rate |
|
what does sinus tachycardia look like on ECG?
|
>100 bpm with every p followed by QRS, and every QRS followed by p
impulses originate at SA node at rapid rate |
|
what is sinus arrhythmia?
|
impulses originate at SA node at a varying rate
|
|
what is important to look for in a first degree AV block?
|
PR interval > 0.2 sec
|
|
what is important to look for in a second degree AV block?
|
intermittent interception of the sinus impulse
Mobitz type I - progressive prolongation of PR interval, until eventually QRS complex is dropped Mobitz type II - PR interval stays the same, but QRS complex is occassionally dropped |
|
what is important to look for in a third degree AV block?
|
frequency of QRS complexes is lower than that of P waves
same interval between P waves same interval between QRS complexes no set relationship between P waves and QRS complexes |
|
what is a third degree AV block?
|
3rd degree block is a complete block of the AV node
impulses originate at both the SA node and below the site of the block, conducting to the ventricles atria and ventricles depolarize independently, QRS complexes less frequent than P waves |
|
what are the symptoms of third degree AV block?
|
low HR, low BP, poor circulation, difficulty exercising
|
|
what is important to look for in a venticular block?
|
wide QRS complex (>1 large box)
complete block (>0.12 sec) incomplete block (0.1-0.12 sec) |
|
what is a right bundle branch block?
|
electrical impulses leave His bundle, enter left bundle branch only, carried to left ventricle
from left ventricle, spreads to right |
|
how does a right bundle branch block present in EKG?
|
prolongation of last part of QRS complex
MEA shifted slightly to the right terminal R wave in V1 slurred S wave in V6 |
|
what is a left bundle branch block?
|
electrical impulses leave His bundle, enter right bundle branch only, carried to right ventricle
from right ventricle, spreads to left |
|
how does a left bundle branch block present in EKG?
|
widens entire QRS complex
shifts MEA left QS or rS complex in V1 monophasic R in V6 |
|
what causes reentry?
|
a block, creating two alternative pathways around it
one pathway, alpha, is slower than the other, beta when depolarization from slow portion reaches area of fast conduction, it goes back up the other side |
|
what is atrial tachycardia?
|
aka supraventricular tachycardia
initiated in SA node, atria, or AV node; caused by enhanced automaticity of ectopic pacemaker |
|
what is paroxysmal atrial tachycardia?
what are the causes of paroxysmal atrial tachycardia? |
reoccuring sudden onset of tachycardia
1 - AV node abnormality with rapid impulses creates tachycardia >200 bpm 2 - extra tissue which causes short circuits (Wolff Parkinson White Syndrome) |
|
what is Wolff Parkinson White Syndrome?
|
heart condition in which an extra electrical pathway in the heart which causes episodes of tachycardia
with certain types, children are at risk for sudden death esp. with exercise (heart beats so fast, >400bpm, that it doesn't pump blood at all) |
|
what are the treatments for Wolff Parkinson White Syndrome?
|
for episodes of tachycardia, children are encouraged to put face in bucket to activate PS system
for permanent treatment, radio frequency ablation using a catheter |
|
what are the characteristic EKG findings in Wolff Parkinson White Syndrome?
|
short PR interval
delta wave (slurred upstroke of QRS complex) long QRS complex |
|
what is atrial flutter?
|
fast and unsynchronized contraction of atria (multiple P waves between QRS complexes)
P waves are saw tooth flutter waves have constant amplitude, duration and morphology ventricles do not beat as fast (AV node safety valve) usually 2:1 or 4:1 block |
|
what is the difference between atrial flutter and atrial fibrillation?
|
atrial flutter is slower and constant
atrial fibrillation is faster and irregular; generally can't tell P waves apart |
|
what causes atrial flutter and atrial fibrillation?
|
reentry pathways
(regular in flutter and irregular in fibrillation) |
|
how is rapid heart rate (atrial fibrillation) perceived?
|
palpitations
angina, shortness of breath, edema |
|
what is ventricular fibrillation?
|
uncoordinated contractions, so no blood is pumped
considered a medical emergency, causing cardiac arrest and sudden cardiac death caused by ischemic heart disease |
|
what feeling is caused by a premature ventricular complex?
|
palpitations or "skipped beat"
common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, mitral valve prolapse |
|
what can cause premature ventricular contraction?
|
altered automaticity of SA node
ectopic pacemakers and re-entry circuits triggered activity |
|
what are the important features of myocardial cell structure?
|
branching and recombining of fibers forming a latticework
intercalated disks, gap junctions, desmosomes create functional syncytium no skeletal attachment allows it to function over wide range of length foot structures not only between T-tubule and SR, but also between sarcolemma and SR larger T-tubules than skeletal muscle |
|
what are the three differences between excitation-contraction coupling in skeletal muscle vs. cardiac muscle?
|
an isoform of TnT increases the calcium sensitivity in newborns
an isoform of TNI can be phosphorylated and decreases calcium sensitivity Na/Ca exchanger in the sarcolemma in addition to Ca-ATPase to remove Ca |
|
what is the influence of the sympathetic system on stroke volume?
|
NE phosphorylates Ca channels, increases trigger Ca
phosphorylation of phospholamban leads to increased SR Ca-ATPase activity, more Ca for next beat |
|
what is the influence of the parasympathetic system on stroke volume?
|
decrease in Ca influx decreases trigger Ca
increase in K flow through muscarinic channels, which causes shorter AP |
|
what is the mechanism of hypocalcemia?
|
decreases calcium influx during AP
decreases inotropic state decreases peak force decreases shortening velocity decreases stroke volume increases systolic end volume increases end diastolic volume |
|
what is the effect of digitoxin and digoxin?
what are they used for? what class of drug are they? |
blocks Na/K pump
less Na pumped from cell intracellular Na increased Na gradient decreased energy for Na/Ca countertransport decreased decreased extrusion of Ca intracellular Ca increased contractility increased used to treat congestive heart failure and cardiac arrhythmias class = cardiac glycosides |
|
what is the mechanism of digitalis poisoning?
|
Ca buffer overflow
mitochondrial Ca uptake inhibition of ATP production contractility decreased |
|
what is a treppe?
|
staircase phenomenon which compensates for decreased filling time with increased heart rate
|
|
what is a postextrasystolic potentiation?
|
a pause augments the force of the next beat
after an extra beat, the force of the next beat is increased |
|
at what length of overlap can the maximum force be created by cardiac muscle fibers?
|
2.2 um overlap between thick and thin filaments
|
|
what effect does muscle length have on troponin C?
|
increased muscle length increases calcium-sensitivity of TnC
|
|
what effect does muscle length have on calcium release?
|
increased muscle length increases calcium release from SR
|
|
on what does the EDV (preload) depend?
|
end-diastolic pressure
blood volume ventricular compliance |
|
what is the effect of a regurgitant aortic valve?
|
increases preload
|
|
what is the effect of a stenotic mitral valve?
|
decrease preload
|
|
what is the effect of pulmonary hypertension?
|
increases preload
|
|
what is the effect of hemorrhage?
|
decreased preload
decreased CO |
|
what is afterload?
|
force against which the ventricle must contract to eject blood
tension produced by a chamber of the heart in order to contract pressure that has to be generated by the chamber of the heart to eject blood from the chamber |
|
by what is afterload estimated?
|
MAP
|
|
what is stroke volume?
|
volume ejected by one beat of the heart (50-70mL)
SV = EDV - ESV EDV - volume in ventricle before ejection ESV - volume in ventricle after ejection |
|
what is the formula for ejection fraction?
what is a normal ejection fraction? |
EF = (SV / EDV) x 100
normal is about 55% peak training can get to 90% |
|
what is the equation for cardiac output?
what is a normal cardiac output? |
CO = SV x HR
normal is about 5-6 L/min |
|
what is the Frank Starling Mechanism?
|
increasing venous return to the heart stretches the ventricle, which in turn results in more forceful ejection of blood at next heartbeat
|
|
in a Frank Starling plot what are the independent and dependent variables?
|
independent - EDV/atrial pressure
dependent - SV/CO |
|
how does positive inotropy affect a Frank Starling Plot?
|
moves the curve up and left
|
|
how does negative inotropy affect a Frank Starling Plot?
|
shifts the curve down and right
|
|
what is the equation for stroke work?
what is the equation for cardiac minute work? |
stroke work = aortic pressure x SV
cardiac minute work = aortic pressure x SV x HR |
|
what is the equation for rate pressure product?
|
RPP = aortic pressure x HR
aka double product estimate that assumes constant SV |
|
what affects myocardial oxygen consumption (MVO2)?
|
heart rate
wall tension |
|
what equation estimates wall tension?
what is the equation? |
Law of LaPlace
P = 2HT / r P = pressure H = wall thickness T = stress = strength r = radius HT = wall tension |
|
what is the upper curve of the ventricular performance pressure volume loops?
|
relationship between ventricular pressure during systole and EDV
indicates maximal possible pressure for a given volume during systole |
|
what is the lower curve of the ventricular performance pressure volume loops?
|
relationship between ventricular pressure and ventricular volume during diastole
coincides with ventricular filling phase |
|
where do the valves open and close in a ventricular performance pressure volume loop?
|
mitral opens at lower left
mitral closes at lower right aortic opens at upper right aortic closes at upper left |
|
what effect does increased preload have on a ventricular performance pressure volume loop?
|
increased filling shifts right side of the loop to further right
max systolic pressure gets somewhat higher |
|
what effect does increased afterload have on a ventricular performance pressure volume loop?
|
whole curve shifts right, narrows, and gets taller
entire bottom line slopes up |
|
what effect does increased contractility have on ventricular performance pressure volume loops?
|
shifts left side of loop farther left
increases max systolic pressure |
|
what is estimated by the area under a ventricular performance pressure volume loop?
|
cardiac work or stroke work
SW = MAP x (EDV - ESV) |
|
for what is the Fick Principle useful?
|
calculating body oxygen consumption and/or relating it to cardiac output
CO = Body O2 Consumption / (O2PV - O2PA) |
|
what is thermodilution?
|
a Swan-Ganz catheter is used to inject cold saline upstream
a thermistor at the tip of the catheter measures the temperature so you can determine the amount of time for the blood temp to return to normal |
|
what is a cardiac cycle?
|
the sequence of electrical and mechanical events occurring in a single heart beat
|
|
how does the timing of events in the left heart compare to the timing in the right heart?
|
happens more or less simultaneously
only difference is that everything is at a higher pressure in the left heart |
|
what are the two forces which contribute to ventricular filling?
|
atrial kick (less important)
active ventricular relaxation (major force) |
|
what causes the first heart sound?
|
sound of the AV valve closing
|
|
what causes the second heart sound?
|
sound of the aortic and pulmonic valves closing
|
|
what are the different steps of cardiac contraction?
|
1 - atrial systole
2 - isovolumetric ventricular contraction 3 - rapid ventricular ejection 4 - reduced ventricular ejection 5 - isovolumetric relaxation 6 - rapid ventricular filling 7 - reduced ventricular filling |
|
what causes the third heart sound?
|
rapid ventricular filling
***this sound is abnormal*** |
|
what is the longest phase of the cardiac cycle?
|
reduced ventricular filling
|
|
where are beta1 receptors found?
|
cardiac muscles
|
|
where are alpha1 receptors found?
|
peripheral vasculature
|
|
where are beta2 receptors found?
|
muscular vascularization
|
|
what are the dependent and independent variables in a cardiac and vascular function curve?
|
dependent - CO & VR
independent - EDV & RAP |
|
what is an equilibrium point in cardiac and vascular function curves?
|
point where the two curves intersect, which occurs when cardiac output is equal to venous return
|
|
what is the effect of positive inotropic agents on cardiac and vascular function curves?
|
increase contractility
increase CO equilibrium point shifts to higher CO and lower RAP |
|
what is the effect of negative inotropic agents on cardiac and vascular function curves?
|
reduce contractility
reduce CO equilibrium point shifts to lower CO and higher RAP |
|
what can change mean systemic pressure?
|
increased by increase in blood volume
increased by decrease in venous compliance |
|
what is the effect, on a cardiac and vascular function curve, of an increase in mean systemic pressure?
|
shifts the venous return to the right
|
|
what happens to the curves in a cardiac and vascular function curve when TPR is increased?
|
CCW rotation of venous return curve
CW rotation of cardiac output curve |
|
what can cause a splitting of S1?
|
mitral valve closes slightly before the tricuspid valve (usually not heard, but loudest at heart apex)
can be exaggerated because of a right bundle branch block or something else which delays the closing of the tricuspid valve |
|
what can cause a splitting of S2?
|
aortic valve closes slightly before pulmonic valve
inspiration increases splitting splitting can be fixed if patient has atrial septal defect or ventricular septal defect reversed splitting (disappears with inspiration and comes back with expiration) patient could have aortic stenosis, left bundle branch block, left ventricular hypertrophy, or anything that delays closing of aortic valve |
|
when can one hear S4?
|
atrial systole
|
|
what can cause murmurs?
|
valve not closing tightly
blood flowing through narrowed opening or stiff valve abnormal holes are present (e.g. septal defects) heart is infected |
|
what is the rating scale for heart murmurs?
|
I - Lowest intensity, difficult to hear even by expert listeners
II- Low intensity, but usually audible by all listeners III - Medium intensity, easy to hear even by inexperienced listeners, but without a palpable thrill IV - Medium intensity with a palpable thrill V - Loud intensity with a palpable thrill. Audible even with the stethoscope placed on the chest with the edge of the diaphragm VI - Loudest intensity with a palpable thrill. Audible even with the stethoscope raised above the chest. |
|
what type of murmur is caused by aortic stenosis?
|
systolic murmur
|
|
what type of murmur is caused by pulmonic stenosis?
|
systolic murmur
|
|
what type of murmur is caused by mitral regurgitation?
|
systolic murmur
|
|
what type of murmur is caused by tricuspid regurgitation?
|
systolic murmur
|
|
what type of murmur is caused by aortic regurgitation?
|
diastolic murmur
|
|
what type of murmur is caused by pulmonic regurgitation?
|
diastolic murmur
|
|
what type of murmur is caused by mitral stenosis?
|
diastolic murmur
|
|
what type of murmur is caused by tricuspid stenosis?
|
diastolic murmur
|
|
what causes sympathetic tone? where is it relatively higher and lower?
|
slow discharge of sympathetic nerve fibersand slow removal of NE
higher in skin and resting skeletal muscle; lower in cerebral and coronary vessels |
|
what is the effect of sympathetic input on large arteries?
|
decrease in compliance
(not change in diameter) |
|
what is nitroprusside?
|
very fast-acting NO-mediated vasodilator used for malignant hypertension
**not used for chronic hypertension since body has already adjusted to an increased sympathetic tone** |
|
what is the effect of low to moderate circulating epinephrine on blood flow?
|
beta2 -> skeletal muscle vasodilation -> redistribution of blood flow to skeletal muscle
beta1 -> increased HR -> increased CO |
|
what is the effect of high circulating epinephrine on blood flow?
|
alpha1 -> vasoconstriction -> minor change in MAP
|
|
what is the mechanism by which circulating norepinephrine works? how is this paradoxical?
|
alpha1 -> vasoconstriction -> increased MAP -> stimulation of baroreceptors -> reflex cardiac slowing -> decreased HR -> decreased CO
NE increases HR when released as a neurotransmitter |
|
where are the main sensors for the baroreceptor reflex?
what is their firing pattern? |
carotid sinuses and aortic arch
frequency of firing increases during systole and decreases during diastole |
|
what is a Valsalva test?
how is it useful? |
exhale with mouth and nose shut and then start breathing normally
used to monitor ANS control of the heart |
|
what happens to arterial BP during sleep?
|
falls 10-20 mmHg, but vasomotor center ignores it and makes no attempt to correct it
|
|
where is renin produced/released?
|
juxtaglomerular cells in the afferent arterioles (also efferent arterioles to a lesser extent) of the kidney
|
|
what is the macula densa?
|
collection of cells in the distal convoluted tubule of a nephron, which are sensitive to Na concentration and send signals to the juxtaglomerular cells when the Na concentration gets too low
|
|
what is the Renin-Angiotensin-Aldosterone System?
|
system which regulates the amount of fluid volume released in urine and the amount retained in the body?
decreased Na -> renin secretion by JG cells -> cleaves angiotensinogen to angiotensin I -> cleaved by ACE in lungs to angiotensin II -> increases Na and Cl retention, aldosterone secretion, arteriolar vasoconstriction, ADH secretion |
|
from where is angiotensinogen released?
|
liver
|
|
where is angiotensin I converted to angiotensin II?
how? |
surface of pulmonary and renal endothelium
enzymatic activity of angiotensin converting enzyme (ACE) |
|
how do angiotensin II, AVP, and catecholamines maintain arterial pressure?
|
reinforce sympathetic mediated vasoconstriction by increasing systemic vascular resistance and decreasing venous compliance
|
|
how do angiotensin II, aldosterone, and AVP increase blood volume?
|
increase water resorption in kidneys
|
|
how are central chemoreceptors stimulated?
|
***high PCO2***
low PO2 |
|
where are central chemoreceptors?
|
in medulla
|
|
where are peripheral chemoreceptors?
|
carotid body
aortic body |
|
by what are peripheral chemoreceptors stimulated?
|
***low PO2****
high PCO2 of arterial blood low flow through bodies block of oxidative metabolism |
|
what is the overall effect of central and peripheral chemoreceptors?
when are these chemoreceptors important? |
positive chronotropy
positive inotropy arteriolar vasoconstriction important more for extreme and chronic situations than for normal cardiac function |
|
what is the effect of stagnant hypoxia in carotid bodies?
|
enhances peripheral vasoconstriction
|
|
what is considered extreme hypotension?
regulation by what mechanism is important in this situation? |
MAP < 60mmHg
regulation of BP by chemoreceptors |
|
what are the stimuli for the release of ANP?
|
atrial distention
sympathetic stimulation angiotensin II endothelin |
|
what is the function of neutral endopeptidase (NEP)?
|
to degrade ANP, thereby increasing BP
|
|
for what are NEP inhibitors used?
|
hypotensive drug in heart failure
inhibits the degradation of ANP, so that excess fluid can still be eliminated through the kidneys |
|
what are the effects of ANP?
|
increase glomerular filtration rate, decreasing blood volume, decreasing CVP, decreasing CO, decreasing MAP
decrease CVP directly, decreasing CO, decreasing MAP decrease SVR (vasodilation), decreasing MAP |
|
what is SVR?
|
systemic vascular resistance
|
|
what is the importance of ANP?
|
counter-regulatory system for RAAS
|
|
what is BNP?
|
brain natriuretic peptide
hormone released by and acting through essentially same mechanism as ANP, though it is released from the ventricles and the brain |
|
how is BNP useful clinically?
|
diagnostic marker for heart failure
|
|
what is the bainbridge reflex?
|
increase in HR, caused by increased CVP and triggered by cardiopulmonary baroreceptors in atria, veins, and pulmonary vessels
|
|
what is a proprioceptor reflex?
|
increase in HR stimulated by muscle and joint movement
|
|
what is nipride?
|
NO-mediated drug
(same as nitroprusside) |
|
what are metropolol and esmolol?
|
beta blocker
(esmolol has rapid onset) |
|
what is atavan?
|
anticonvulsant
tranquilizer |
|
what is the effect of cocaine on the circulatory system?
|
mimics the sympathetic system
|
|
as a drug, what is epinephrine?
|
alpha and beta adrenergic agonist
|
|
what is phenolamine?
|
alpha adrenergic agonist
|
|
what are the drugs used to treat stage 1 hypertension?
|
thiazide diuretic
lifestyle changes plus 1: Beta blocker Ace inhibitor Angiotensin II receptor blocker Calcium channel blocker |
|
what are the drugs used to treat stage 2 hypertension?
|
thiazide diuretic
lifestyle changes plus 2: Beta blocker Ace inhibitor Angiotensin II receptor blocker Calcium channel blocker |
|
what is defined as stage 1 hypertension?
|
140-159 / 90-99
|
|
what is defined as stage 2 hypertension?
|
>160 / >100
|
|
what are the functions of microcirculation?
|
exchange nutrients, water, gases, hormones, and waste between blood and cells
regulation of vascular resistance |
|
what is the name for the vessels that supply capillaries?
|
terminal arterioles
|
|
how do arterioles make up such a high percentage (70-80%) of total vascular resistance?
|
can constrict to 40-50% from resting diameter for long periods of time
can dilate 60-100% from resting diameter |
|
what type of ANS receptors are found on arterioles?
|
alpha1 receptors only
|
|
how does the Law of Laplace apply to a blood vessel?
|
HT = P x r
HT = wall tension = wall thickness x wall stress the larger the vessel radius, the larger the wall tension for a given pressure |
|
what is the primary site of water and solute exchange?
|
capillaries
|
|
what are pericytes?
|
aka Rouget cells
possibly a primitive form of vascular smooth muscle cells which add structural integrity to capillaries |
|
what is the Lindqvist effect?
|
apparent viscosity of blood is decreased as it flows through a smaller diameter vessel (e.g. capillary), because erythrocytes travel in center and plasma travels along walls
|
|
by what are endothelial cells of the capillary wall held together?
|
tight junctions, with occasional gaps
|
|
what types of molecules pass easily through capillary walls and which are more difficult?
|
lipid-soluble molecules (O2, CO2) easily pass by simple diffusion
small water soluble molecules (glucose, amino acids) must diffuse through water filled pores or clefts between endothelial cells |
|
what type of molecules are retained within capillaries?
|
large, water-soluble substances (albumin, antibodies, complement)
can cross by pinocytosis, or limited number of large pores |
|
what acts as a filter for large pores of capillaries?
|
submicron fibers
|
|
how does Fick law apply to capillaries?
|
it is an equation to calculate the flux (diffusion), and diffusion is by far the most important means for moving substances across capillary walls
indicates that the rate of diffusion depends on vascular permeability, surface area, and concentration difference |
|
what is an extraction ration?
|
E = (Ca - Cv) / Ca
Ca - arterial concentration Cv - venous concentration always less than one (+) if material removed from blood - filtration (-) if material is added to the blood - reabsorption |
|
what is the starling equation?
|
Jv = Kf [( Pc - Pi ) - sigma ( pic - pii )]
Jv - net fluid flux Kf - filtration coefficient - hydraulic conductance Pc - capillary hydrostatic pressure Pi - interstitial hydrostatic pressure sigma - reflection coefficient pic - capillary oncotic pressure pii - interstitial oncotic pressure |
|
what is the net driving pressure?
|
( Pc - Pi ) - sigma ( pic - pii )
|
|
what are the primary forces for fluid filtration and absorption across capillary walls?
|
capillary hydrostatic pressure (Pc)
capillary oncotic pressure (pic) |
|
why is reabsorption more prominent than filtration at the venous end of capillaries, when filtration is more prominent than reabsorption at the arterial end?
|
the net filtration pressure is dependent on the net hydrostatic pressure and the net osmotic pressure
capillary hydrostatic pressure (BP) is much higher on arterial end than on the venous end capillary hydrostatic pressure is the only pressure to change, and since it gets so small, the net osmotic pressure overwhelms it at the venous end |
|
what proportion of filtered fluid reenters the capillaries?
what happens to the rest? |
9/10 reenters capillaries
other 1/10 enters lymphatic circulation |
|
what happens during left ventricular failure or mitral valve stenosis?
|
pulmonary capillary hydrostatic pressure > plasma oncotic pressure
leads to pulmonary edema |
|
what happens to filtration in pregnancy and right ventricular failure?
|
elevated CVP increases filtration beyond capacity of lymph system to remove
leads to ankle edema |
|
what happens to filtration in hepatic cirrhosis?
|
elevated hepatic vascular resistance causes elevated portal venous pressure and elevated capillary pressure in splanchnic circulation
causes ascites |
|
what happens to filtration in dehydration?
|
elevated conc. of plasma protein causes increase water resorption into vessels
|
|
what happens to filtration in nephrosis?
|
decreased conc. of plasma proteins
causes edema |
|
what happens to filtration in severe burns?
|
increased capillary permeability causes increased water filtration into tissues
|
|
how do smooth muscle cells of venules differ from those in arterioles?
|
much smaller in diameter
longer |
|
what portion of the blood is in the venous system at rest?
|
2/3
|
|
why are smallest venules more permeable than capillaries?
|
bigger pores
|
|
what are varicose veins?
what problems can be associated with them? |
visibly enlarged veins that are often bluish in color and may appear twisted
cosmetic problem phlebitis thrombophlebitis deep vein thrombosis |
|
what is phlebitis?
|
inflammation of a vein
|
|
what is thrombophlebitis?
|
inflammation of a vein with a blood clot
|
|
what is deep vein thrombosis?
|
aka DVT
blood clot in a deep vein that can break away, lodge in the lungs, and become life threatening |
|
as what do lymphatic vessels begin?
how does fluid enter the lymphatic vessels? |
blind-ended lymphatic bulbs
fluid from tissue moves passively into vessel lumen |
|
what allows lymph vessels to "suck up" lymph?
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compression-relaxation cycle
valves in lymphatic vessels |
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how much does the pressure change between bulbs/small vessels and the larger vessels?
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from only a few mmHg to 10/20 mmHg
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what allows lymph to flow up a pressure gradient?
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contraction of larger lymphatic vessels
lymph valves that avoid back flow |
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how much fluid does the lymphatic system collect in a day?
what does it do with the fluid? |
about three liters
filters it through lymph nodes and then returns it to the blood at the junction of the internal jugular vein and left subclavian vein |
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what is the myogenic mechanism of autoregulation?
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smooth muscles in the walls of arterioles open ion channels, depolarize, and contract in response to stretch
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what is active hyperemia?
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concept that blood flow to an organ is proportional to its metabolic activity
increased blood flow when tissue is active |
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what is reactive hyperemia?
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transient increase in organ blood flow that occurs following a brief period of ischemia, which corrects for the shortage of oxygen and build-up of metabolic waste
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when can reactive hyperemia be seen?
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transient coronary occlusions (coronary vasospasm)
removal of a tourniquet release of arterial clamp during surgery |
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what are the mechanisms by which reactive hyperemia occurs?
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accumulations of metabolites
up and down regulation of sympathetic tone histamine and bradykinin - local edema serotonin - vasoconstriction in response to vascular blood loss prostaglandins - E is dilator, F is constrictor |
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what is the distribution of blood flow at rest?
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kidney - 20%
heart - 5% brain - 15% skeletal muscle - 20% skin - 5-10% |
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what is the maximum blood flow increase of kidneys?
heart? brain? skeletal muscle? skin? |
constant
4-5 fold constant 20-30 fold up to 100 fold |
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what sections of the heart are supplied by the right coronary artery?
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right atrium
SA node right ventricle bottom of left ventricle |
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what sections of the heart are supplied by the left coronary artery?
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majority of left ventricle
|
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what sections of the heart are supplied by the posterior descending artery?
from where does it branch? what artery replaces it in 20% of people? |
posterior left ventricular wall
right coronary artery circumflex artery |
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in what location can you tell there is an infarct for each of the limb leads of an EKG?
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lead 1 - lateral infarct
lead 2 - inferior infarct lead 3 - inferior infarct |
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what is important about the blood supply of the heart?
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crucial, because heart is limited to oxidative metabolism
extraction of oxygen is highly efficient in heart blood flow is about 225mL/min at rest and 4-5 times that during exercise blood flow slightly decreases during systole, and slightly increases during diastole |
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what is the response of coronary arteries to hypoxia?
to adenosine, protons, and CO2 (chemicals released by cardiac cells)? to NO (chemicals released by endothelial cells)? |
vasodilates in response to all of these
|
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how do coronary arteries respond to sympathetic regulation?
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equalize blood flow through the heart layers (alpha1-receptor dependent vasoconstriction)
suppress decrease in resistance during exercise (beta-receptor dependent vasodilation) |
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what cardiac enzymes are released by a damaged heart?
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cTnI (troponin I)
cTnT (troponin T) creatine kinase myoglobin lactic dehydrogenase |
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what are the isoforms of creatine kinase?
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CK-MB1 - released by heart muscle
CK-MB2 - released by heart muscle and converted to MB1 in blood CK-MM - in skeletal muscle CK-BB - in brain |
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what are the key concepts of coronary circulation?
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ability of heart muscle to pump blood depends almost exclusively on O2 supplied by coronary microcirculation
most important regulators are local metabolic factors (e.g. hypoxia, adenosine) |
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what is an adaptation the cardiovascular system makes in response to heart failure after MI?
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expansion of blood volume, which thereby increases CVP and RAP
|
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what is caused by cerebral ischemia of a few seconds?
of a few minutes? |
loss of consciousness
irreversible brain damage |
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what are the factors affecting regulation of cerebral blood flow?
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autoregulation (between 60 and 160 mmHg)
local factors (CO2, pH, adenosine, K) ****mainly CO2**** |
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what is the effect of CO2 on the cerebral circulation?
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moderate increase - vasodilation
large increase - vasoconstriction |
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why is CO2 the major local factor that regulates cerebral blood flow?
|
passes blood-brain barrier well, whereas other things like protons do not
|
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what are the key concepts of the cerebral circulation?
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blood flow increases when neurons are active and require additional oxygen
most important local vasodilator is CO2 |
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from where do the branchial arteries originate?
what is their function? |
thoracic aorta
provide nutrients to tracheo-bronchial tree down to the terminal bronchioles |
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from where do the pulmonary arteries originate?
what is their function? |
right ventricle
gas exchange |
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why do the walls of the pulmonary vasculature have less smooth muscle than does the systemic vasculature?
|
low resistance and low pressure system
|
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what has the most important influence on pulmonary vasomotor tone?
what is the effect of this stimulus? |
hypoxia
vasoconstriction (opposite what happens in systemic circulation) |
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what are the regulators of pulmonary vasculature?
|
hypoxia - vasoconstriction
ANS angiotensin II - pulmonary arterioles constrict serotonin - pulmonary venules constrict histamine - pulmonary venules constrict |
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what are the key concepts of the pulmonary circulation?
|
object of autoregulation is to route blood to best ventilated alveoli
increased oxygen causes vasodilation decreased oxygen stimulates vasoconstriction |
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what are the effects of PS activation on small intestine blood flow?
|
****increased secretion -> increased metabolites -> increased vasodilation -> increased blood flow****
increased motility -> increased mechanical resistance -> decreased blood flow |
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what are the circulating/metabolic constrictors of small intestine circulation?
|
stress mediators, "sacrificing" GI activity
NE epinephrine dopamine angiotensin II vasopressin |
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what are the circulating/metabolic dilators of small intestine circulation?
|
mediators of GI activity
vasoactive intestinal peptide (VIP) gastrin colecystokinin glucagon |
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what are the effects of sympathetic activation on the gastrointestinal circulation?
|
****alpha-adrenergic vasoconstriction -> decreased perfusion of villi -> necrosis of villi -> inflammation and sepsis****
relaxation of intestinal muscle -> decreased mechanical resistance -> increased blood flow |
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to what does the term mesenteric circulation refer?
|
vasculature of the intestines
|
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to what does the term splanchnic circulation refer?
|
vasculature to abdominal portion of digestive system
|
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into what vein does the splenic vein empty?
|
portal vein
|
|
what are the key concepts of the gastrointestinal circulation?
|
regulation during nutrient absorption depends on PS, GI hormones, and increased cellular metabolites
liver receives portal venous blood from GI organs as its main blood supply, supplemented by hepatic arterial blood |
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what is the main task of the cutaneous circulation?
|
thermoregulation
|
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what is the sole innervation of the cutaneous circulation?
|
sympathetic innervation
|
|
what are the stimuli for the cutaneous circulation?
|
E and NE - vasoconstriction - shunt blood to core - activates sweat glands (release bradykinin and vasodilates)
increased core temperature - vasodilation before sweating starts increased local skin temp - vasodilation via local metabolic and myogenic autoregulation |
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what is the sole regulator of arteriovenous anastomoses in the hands, feet, lips, ears, and nose?
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exclusively autonomic nervous system (no metabolic regulators)
|
|
why are arteriovenous anastomoses in the hands, feet, lips, ears and nose so important?
|
contribute a lot to thermoregulation due to ability to completely constrict and its high level of adjustability (constrict to 1/10 of normal during cold exposure and dilate to 10 times normal during heat exposure)
|
|
what is countercurrent heat exchange in the cutaneous circulation?
|
in cold - cooled venous blood goes directly to arteries before they reach the surface
in heat - heat from surface is given from veins to colder arterial blood |
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what are the key concepts in cutaneous circulation?
|
skin has low O2 requirement, by high blood flow during warm temperatures or exercise supplies a large amount of heat for dissipation to external environment
sympathetic stimulation of heart and blood vessels also results in shunting blood away from skin |
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how does muscle tissue oxygen consumption at rest compare to cardiac muscle and brain tissue?
|
lower oxygen consumption in resting muscle tissue per gram than brain and heart muscle
|
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what are the regulators of muscle vasculature?
|
sympathetic innervation of arterioles
regulation by local factors (dominate during excercise) |
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what are the effects of sympathetic innervation on muscle arterioles?
|
alpha1 receptors - vasoconstriction
beta2 receptors - vasodilation |
|
what are the local factors that regulate muscle circulation?
|
hypoxia
adenosine lactic acid H+ CO2 K+ NO |
|
how is blood redistributed during exercise?
|
brain maintains constant flow
heart needs increases 3 fold skeletal muscle increases 10 fold skin increases 4 fold for heat regulation kidney decreases by 1/2 GI decreases by 1/2 |
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in what order is blood diverted during exercise?
|
skin -> GI -> renal
blood returns to skin when body heat increases too much |
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what are the key concepts for skeletal muscle circulation?
|
skeletal muscle tissue receives minimal blood flow at rest because of its limited oxygen requirements, but flow and oxygen use can increase 10-30 fold during intense activity
|
|
what creates the constant flow in renal circulation when the MAP is between 75 and 175 mmHg?
|
myogenic response
tubuloglomerular feedback glomerular filtration rate |
|
how much of the blood supply of the kidney supplies the cortex? the medulla?
|
80% to cortex
20% to medulla (of the 20% total blood flow of the kidney) |
|
what are the two vascular beds of the kidneys?
|
glomerular capillaries
peritubular capillaries |
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what is the function of counter-current flow in the medulla of the kidney?
|
maintains cortex-medulla osmotic gradient
|
|
what are the key concepts of the renal circulation?
|
receives the highest blood flow per gram
as blood flows through kidneys, its composition is appropriately altered according to homeostatic requirements blood flow to kidneys is dependent on systemic blood pressure and intra-renal vascular resistance (autoregulated) |
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when is the first heartbeat of a fetus?
|
21-22 days after conception
|
|
when do coordinated contractions of the fetal cardiovascular system result in unidirectional flow?
|
end of week 4
|
|
when does the SA node develop in a fetus?
|
week 5
|
|
what vessel carries oxygenated blood to the placenta?
|
spiral arteries
|
|
what vessel carries deoxygenated blood away from the placenta?
|
endometial vein
|
|
what vessel carries oxygenated blood away from the placenta?
|
umbilical vein
carries O2 and nutrients from mother's blood to baby |
|
what vessel carries deoxygenated blood toward the placenta?
|
umbilical artery
carries baby's waste and CO2 to mother's blood |
|
how much of the mother's resting cardiac output is diverted to the fetus at the end of gestation?
|
15-25%
|
|
what is the path of blood through fetal circulation?
|
umbilical vein -> portal vein -> ductus venosus -> inferior vena cava -> right atrium -> foramen ovale -> left atrium -> left ventricle -> aorta -> umbilical artery
if blood misses foramen ovale: right atrium -> right ventricle -> pulmonary artery -> ductus arteriosus -> aorta -> umbilical artery if blood misses ductus arteriosus: pulmonary artery -> pulmonary vein -> left atrium -> left ventricle -> aorta -> umbilical artery |
|
what are the three shunts of the fetal circulation?
where are they? what do they bypass? |
ductus venosus - between portal vein and IVC - bypasses liver
ductus arteriosus - between pulmonary artery and descending aorta - bypasses lungs foramen ovale - between right atrium and left atrium - bypasses entire pulmonary circulation |
|
how is the cardiac output of a fetal heart calculated?
|
CO = COLV + CORV
CO - cardiac output COLV - cardiac output from left ventricle CORV - cardiac output from right ventricle |
|
what happens at birth to the newborn's pulmonary system?
|
lungs inflate
decreased pulmonary vascular resistance decreased pulmonary pressure hypertrophy of right ventricle subsides constriction of peripheral arterioles due to higher oxygen concentration and sympathetic hypertrophy of left ventricle develops PO2 dilates lung vessels and constricts ductus arteriosus |
|
when do the three fetal circulatory shunts close?
|
ductus arteriosus - at birth
foramen ovale and ductus venosus - 2-3 months after birth |
|
what are the key concepts of fetal circulation?
|
fetus obtains nutrients and oxygen from mother's blood supply, using combined maternal and fetal placental circulations
heart chambers have radically different roles in pumping blood between fetus and adulthood designed to carry oxygenated blood from placenta to fetal circulation by bypassing the lungs three fetal ducts (DA, FO, DV) must be closed after birth |