Physiology Flashcards
Three pressures in the CV system?
- Driving (difference between two points)
- Hydrostatic (P of gravity and weight of blood)
- Transmural (P of blood on vessel wall)
Arteriolar resistance is regulated by the _1_ nervous system.
- Autonomic
Arteries are under _1_ pressure and Veins are under _2_ pressure.
- High
- Low
Blood flows from __1 (high/low)__ pressure to __2 (high/low)__ pressure. The __3__ drives blood flow.
- High
- Low
- Pressure gradient
Blood flow is inversely proportional to the _1_ of blood vessels. When blood flow increases, _1_ has decreased.
- Resistance (nothing is holding it back)
What is the equation for blood flow/cardiac output/Q?
CO = (Mean arterial pressure [highest P] - Right arterial pressure [lowest P]) / (Total peripheral resistance [TPR])
What are the factors that change the resistance of blood vessels (3)?
- Viscosity of blood (numerator)
- Length of blood vessel (numerator)
- Radius of blood vessel to the fourth power (denominator)
Resistance = (8*visc*length)/(pi*r^4)
What is viscosity?
Increased viscosity is due to increased internal friction.
- thickness
- the state of being thick, sticky, and semifluid in consistency
- a measure of its resistance to gradual deformation by shear stress or tensile stress
Increasing viscosity by increasing hematocrit will _1_ resistance and _2_ blood flow.
- increase
- decrease
Increasing the length of a vessel will _1_ resistance. Increasing the radius of a vessel _2_ resistance.
- increase
- decrease
If a blood vessel radius decreases by a factor of 2 then resistance _1_ by a factor of _2_ and blood flow _3_ by a factor of _4_.
- increases
- 16
- decreases
- 16
_1_ resistance is illustrated by systemic circulation. Each artery in _1_ receives a fraction of the total blood flow.
Parallel
When an artery is added in parallel, the total resistance _1_. In each parallel artery, the pressure is the _2_.
- decreases
- same
_1_ resistance is illustrated by the arrangement of blood vessels in a given organ. _2_ are the largest contributers to this resistance.
- Series
- Arterioles
As blood flows through the series of blood vessels, pressure _1_. Each blood vessel in series receives the _2_ total blood flow.
- decreases
- same
_1_ flow is streamlined. _2_ flow is not and causes audible vibrations called _3_.
- Laminar
- Turbulent
- bruits
A _1_ number predicts whether blood flow will be turbulent or laminar.
Reynold’s number
An increased Reynold’s number increases the likelihood of _1 (laminar/turbulent)_ flow.
turbulent
What are the two factors that increase a Reynold’s number?
- Decreased blood viscosity (ex. anemia, lower hematocrit)
- Increased blood velocity (ex. narrowing of a vessel [decreased radius)
What is hematocrit?
the volume percentage of red blood cells in blood
Pulse pressure is the difference between _1_ and _2_ presures.
- systolic
- diastolic
Aging leads to a _1_ in capacitacne and an _2_ in pulse pressure.
- decrease
- increase
When is systolic pressure measured?
**After **the heart contracts (systole) and blood is ejected in the **arterial **system.
When in diastolic pressure measured?
When the heart is relaxed (diastole) and blood is returned to the heart via the veins.
Systolic pressure is the _1 (highest/lowest)_ arterial pressure during a cardiac cycle. Diastolic pressure is the _2 (highest/lowest)_ arterial pressure during a cardiac cycle.
- highest
- lowest
Mean arterial pressure = ?
MAP = 1/3 Systolic P + 2/3 Diastolic P
*because most of the cardiac cycle is spent in diastole
Venous pressure is very _1 (high/low)_. Veins have a _2 (high/low)_ capacitance and therefore can hold _3 (large/small)_ volumes of blood at low pressure.
- low
- high
- large
*Capacitance is proportional to volume (numerator) and inversely proportional to pressure. As a person ages, their arteries become stiffer and less distensible/stretchy therefore capacitane of arteries decreases with age.
what are 4 methods of regulating arterial blood pressure?
- Increase pumping force
- contract veins and arterioles
- infuse fluids
- administer vasoconstrictors
which ventricle has a thicker muscular layer? why?
the left ventricle. It must pump blood through to aorta to systemic circulation.
how does the heart contract?
in a spiral contraction (like wringing a washcloth)
what is the % ejection volume referring to?
the amount of blood pushed out of the ventricles
capillaries have (high/low) velocity, (high/low) resistance and (high/low) cross-sectional area.
low
low
high
arterioles have the (highest/lowest) resistance
highest
the x descent on a jugular venous pulse reading is caused by what?
decrease in pressure in the right atrium (after peak of c wave after atrial relaxation)
what are the three types of action potentials? What differentiates the three?
atrial, ventricular, nodal
A/V have cardiac AP phases 0-4 while nodal only has 0, 3, amd 4
what does phase 4 represent in an atrial or ventricular cell?
In a nodal cell?
A/V: resting potential (constant horizontal line)
Nodal: pacemaler potential (not constant)
what does phase 0 represent in cardiac action potentials? what is the acting ion in a/v cells and nodal cells?
rapid depolarization and the start of an AP.
a/v: sodium Na+
nodal: Calcium Ca2+
phase 1 represents the brief, partial _1_ of ventricular and atrial action potentials. This phase is not present in _2_ APs.
- repolarization
- nodal
phase 2 looks different in every cell. It is a _1_ in ventricular cells, _2_ in atrial cells and _3_ in nodal cells.
- plateau
- abbreviated/shorter
- missing
what does phase 3 represent? How is the nodal cell different?
repolarization to return to resting or pacemaker level. It is **slower **in nodal cells (remember long slope required to get to phase 0– in a/v cells, 0 shoots straight up)
what channel is responsible for the phase 4 resting potential?
the inwardly rectifying K+ channel that acts as if it is voltage-gated but is not.
what is the function of the ikr and iks channels?
they open during phase 2 and hekp the cell to repolarize back to resting level
what is a refractory period?
the point where initiation of a new action potential is difficult or impossible.
how does the ik1 inwardly rectifying channel allows a transition to phase 0?
when the membrane is depolarized, Mg and polaymines plug up and partially block the channel therefore less K+ can pass through. This gives calcium and sodium the opportunity to depolarize the cell and maintain AP
what phases are included in the absolute refractory period? justify why.
Pjases 0-2. membrane depolarizes in 0 and the plateau ends by the end of 2
why is the supranormal refractory period associated with arrhythmias?
many of the fast sodium channels have reset and are able to produce a reduced amplitude AP. you don’t want a contraction here becasue the atria have not been able to fill up completely.
a potassium channel (opens/closes) on depolarization and (opens/closes) on repolarization.
opens to let the potsassium out of the cell and make the cell more positive
closes on repolarizatoin to keep potassium in (electrical potential of K+ is approx. -90 mV)
what is the function of funny channels in phase 4 of the nodal action potential?
on hyperpolarization (when all of the potassium channels close) these sodium channels open and contribute to depolarizing the cell from phase 4 to 0 in the next AP round.
what are the two calcium channels and their roles in the nodal action potential?
CaT opens during phase 4 to help depolarize the cell
CaL (long-lasting) is responsible for the big upstroke of the nodal action potential
Vagal stimulation releases _1_ and (increases/decreases) the heart rate.
What is the effect on Na+, Ca2+ and K+ permeability?
Does this de/hyper/re-polarize the cell?
- Ach
- decreases (parasympathetic effects)
- during pacemake potential: decreases Na+ and Ca2+ permeability and increases K+ permeability.
- Hyperpolarizes the cell
In nodal conductance, what is the effect of Ach on threshold?
Ach changes Na+, Ca2+ and K+ permeability and hyperpolarizes the cell. This makes the cell take longer to reach threshold and the heart rate slows
in nodal conductance, sympathetic stimulation releases _1_.
What is the effect on sodium, calcium and potassium permeabilities.
_1_ promotes (re/de/hyper-polarization), (inc/decreases) time btw APs and (inc/decreases) heart rate.
- norepinephrine
- increases sodium and calcium permeability, decreases potassium permeability.
- depolarization
- decreases
- increases
What are the connections for lead 1 on an EKG?
(-) right arm to (+) left arm
What are the connections for lead 2 on an EKG?
(-) right arm to (+) left leg
(right leg is grounded)
What are the connections for lead 3 on an EKG?
(-) left arm to (+) left leg
what does the magnitude of the mean cardiac vector depend on?
the number of individual cells that are in the provess of depolarizing or repolarizing **and ** their orientation w/ respect to each other
what is the mean cardiac vector for each case? (zero/non-zero)
- all cells at rest (repolarized)
- some cells de- and repolariz-ed/ing
- all cells contracted depolarized)
- zero
- non-zero
- zero
whare are the three pacemaker nodes in the heart?
SA node, AV node and the purkinje fibers.
SA node has the fastest spontaneous rate and therefore dominate. If it stops working, the other two can kick in.
what is the Frank-Starling mechanism?
The strength required to contract the ventricles is proportional to the pressure of the end diastolic (filling) volume
why does depolarization slow when going through the AV node?
allows the atria to completely empty into the ventricle
What are the standard EKG leads? How many of each?
3 bipolar limb leads
3 unipolar limb leads
6 unipolar precordial chest leads
why does R wave progression occur in readings of precordial chest leads?
the V1-6 is orientaed in the horizontal plane from the smaller right ventricle to the larger left ventricle.
What differentiates on an EKG of V5-6 precordial chest leads?
They will show a Q wave on the EKG
what does the PR interval indicate?
What can happen if it is prolonged?
the time it take for a signal to pass from the strium to the ventricle.
The signal can die out
What is Wolff-Parkinson-White Syndrome
Where the PR interval is shortened and an extra delta wave is seen on an EKG. Could lead to supraventricular tachycardia
what does a widened QRS indicated
slow electrical conduction through Purkinje Fibers and through the ventricular muscle.
the QT interval represents what? Prolonged QT syndrome increases risk for what?
duration of ventricular action potential.
If prolonged, there is an increased risk for cardiac arrhythmia
How are action potential and heart rate related?
a fast heart rate indicates a shorter action potental.
the mean QRS is normal when there is an upward deflection in which leads?
lead I and II
ischemic cells have a (longer/shorter) AP than normal and (de/re-polarize) faster than normal. This is due to the opening of an extra potassium channel due to metabolic distress
shorter, repolarize
what does subendocardial ischemia look like on an EKG?
ST segment depression
*remember the endocardium is the first to depolarize therefore it will be that last to repolarize
epicardial ischemia looks like what on an EKG?
ST segment elevation
the left ventricle in the shape of a sphere indicate what pathogy?
heart failure
the epicardium gets its blood supply from where?
the endocardium
Calcium binds to _1_. _1_ moves tropomyosin from the _2_ site on the thin actin filament.
- troponin C
- binding
most of the calcium that permits actin-myosin interaction comes from the _1_ _2_ but _3_ calcium is required for the Calcium Indicued Calcium Release (CICR)
- sarcoplasmic
- reticulum
- extracellular
Cardiac performance is determined by which four factors?
- Preload
- Afterload
- Contractility
- Heart Rate
define preload? What is its significance? How is it measure?
- the tension on the myocytes right before contraction.
- It determines the length of the sarcomeres.
- It is measured by measureing the pressure of the end diastolic volume in the ventricles
define afterload.
how is it measured
should afterload increase or decrease during ejection?
- afterload is the tension in the ventricle wall during contraction
- it is proportional to left ventricle systolic pressure
- afterload should decrease during ejection since the radius of the ventricle is shrinking and blood should be flowing out.
increasing preload (increases/decreases) the velocity and extend of shorteneing if afterload is constant.
Increasing afterload has the (same/opposite) effect.
- preload increases velocity and shortening.
- afterload has the opposite effect and is negatively correlated.
when you have too much preload, the system backs up and can cause what?
blood can flow back into the atria and then the pulmonary veins. This will cause you to bleed out into your lungs and oxygen levels decrease.
what is the benefit of a stretched out sarcomere? What can cause sarcomeres to stretch?
- it increases the calciumc binding sites on the sarcoplasm therefore increasing tension and strength of the contraction.
- Increasing preload stretches sarcomeres.
what is contractility? how is it regulated?
the strength of a contraction
beta adrenergic stimulation
beta adrenergic receptors are regulated by what two things?
- the concentration of calcium
- the phosphorylation of proteins
beta adrenergic receptors have what effect on the heart (3)?
- increase rate of contraction
- increase peak force
- increasing rate of relaxation
what binds to the beta adrenergic receptor?
norepinephrine
what four things can increase contractility?
- neural input (norepinephrine)
- increase catechols
- digoxin
- positive inotropic drugs (increase [Ca])
what can reduce contractility (5)?
- acidosis (decrease oxygenated blood)
- ischemia (same as above)
- negative inotropic drug (decrease [Ca])
- calcium channel blockers
- beta-adrenergic blockers
what is the equation for cardiac output?
CO=SV * HR
Cardiac output is equal to stroke volume multiplied b heart rate
how would you increase preload in a patient?
give a patient IV fluids
how are the semilunar and atriventricular valves opened?
high pressure in the ventricles and atria, respectively
what is the difference in ventricular activity for diastole and systole?
diastole is ventricular filling (relaxation), systole is ventricular emptying (contraction)
what is happening during the P wave?
atrial depolarization
What is happening during the T wave?
ventricular repolarization until ventricular relaxation
what is happening during the QRS complex?
ventricular depolarizaton to ventricular contraction
what are the 5 stages of the left ventricular pressure-volume loop?
- isovolumetric contraction
- ejection (period between aortic valve opening and closing)
- isovolumetric relaxation
- rapid ventricular filling (as soon as mitral valve opens)
- slow ventricular filling (right before MV closes)
what is happening in isovolumetric contraction?
beginning of ventricular systole (contraction) but the aortic valve is closed therefore volume does not change but pressure is rising quickly.
*valves are closed because pressure in aorta is higher than pressure in the ventricle
the period of rapid ejection begins when pressure within the ventricle is _1_ compared to the aorta or pulmonary artery?
- greater
In isovolumetric relaxation, there is a _1_ in ventricular pressure.
It ends when there is what kind of relationship between the ventricle and atrium?
- decrease
when the pressure in the ventricle falls below the atrium
What does the a wave represent in the atrium?
atrial contraction.
*follows P wave of EKG
what does the c wave represent?
ventricular contraction
what does the x descent represent (3)?
- ventricular emptying
- thoracic volume and pressure fall
- rapid fall in atrial pressure
what does the v wave represent?
flow of blood from veins to atria.
*long period of time, AV valves are closed
the v wave corresponds roughly with which segment of the EKG?
ST segment
the *y *descent represents what?
- atria draining into the ventricles
- rapid fall in atrial pressure
What does the S1 heart sound represent?
the mitral and tricuspid valves closing
*at this time the AoV and P valve are opening quietly
What are you hearing with the S2 heart sound?
aortic and pulmonary valve closure
*as MV and TV valves open quietly
What are you hearing with the S3 heart sound?
mitral regurgitation (preload is high, pressure in ventricle increases and MV opens as a result of increased pressure)
what are you hearing with the S4 heart sound?
atrial contraction: the left atrium pushing against a stiff left ventricle
- high atrial pressure
- may lead to ventricular hypertrophy
S4 occurs during with segment of the EKG? Which part of the jugular pulse curve?
P-Q interval; a wave (aortic contraction)
S1 occurs during which part of the EKG diagram? jugular pulse?
- QRS complex (mainly RS when isovolumentric contraction ends)
- c wave (ventricular contraction)
S2 occurs during what part of the EKG?
at the end of the T wave when the ventricle has finished emptying
what is normal sinus rhythm?
a normal heart beat of 60-100 beats/minute
while standing or sitting, aspirated material is most likely to go into which bronchus? which segment?
a right lower lobe basilar segment
If there was a mutation in a connexin gene that interfered with gap junction assembly and inhibited efficient cell-to-cell electrical coupling in Purkinje fibers, what would you expect to see?
a widened QRS complex due to slow action potential conduction in the ventricular muscle
for any given afterload, increasing preload usually has the effect of (increasing/decreasing) the velocity of muscle fiber shortening
increasing
Which statement is true?
“the upstroke (phase 0) of the action potential directly triggers calcium release from the sarcoplasmic reticulum”
OR
“increased systolic calcium levels in the cytosol directly correlates with increased contractility”
“increased systolic calcium levels in the cytosol directly correlates with increased contractility”
To determine the mean QRS, what leads are evaluated in an EKG?
Lead I and aVF
If you had an EKG that showed a positive mean QRS axis on Lead I and a negative mean QRS axis on aVF, what is the overall mean QRS axis:
A. 0 to +90 degrees
B. +90 to 180 degrees
C. -90 to 180 degrees
D. 0 to -90 degrees
E. exactly +60 degrees
D. 0 to -90 degrees
If an aortic valve becomes stenotic, the peak systolic pressure would (increases/decreases) and the end systolic volume would (increase/decrease).
increase, increase
