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CPR-Week 1 > Physiology > Flashcards

Physiology Flashcards

1
Q

Three pressures in the CV system?

A
  1. Driving (difference between two points)
  2. Hydrostatic (P of gravity and weight of blood)
  3. Transmural (P of blood on vessel wall)
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2
Q

Arteriolar resistance is regulated by the _1_ nervous system.

A
  1. Autonomic
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3
Q

Arteries are under _1_ pressure and Veins are under _2_ pressure.

A
  1. High
  2. Low
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4
Q

Blood flows from __1 (high/low)__ pressure to __2 (high/low)__ pressure. The __3__ drives blood flow.

A
  1. High
  2. Low
  3. Pressure gradient
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5
Q

Blood flow is inversely proportional to the _1_ of blood vessels. When blood flow increases, _1_ has decreased.

A
  1. Resistance (nothing is holding it back)
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6
Q

What is the equation for blood flow/cardiac output/Q?

A

CO = (Mean arterial pressure [highest P] - Right arterial pressure [lowest P]) / (Total peripheral resistance [TPR])

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7
Q

What are the factors that change the resistance of blood vessels (3)?

A
  1. Viscosity of blood (numerator)
  2. Length of blood vessel (numerator)
  3. Radius of blood vessel to the fourth power (denominator)

Resistance = (8*visc*length)/(pi*r^4)

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8
Q

What is viscosity?

A

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
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9
Q

Increasing viscosity by increasing hematocrit will _1_ resistance and _2_ blood flow.

A
  1. increase
  2. decrease
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10
Q

Increasing the length of a vessel will _1_ resistance. Increasing the radius of a vessel _2_ resistance.

A
  1. increase
  2. decrease
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11
Q

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_.

A
  1. increases
  2. 16
  3. decreases
  4. 16
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12
Q

_1_ resistance is illustrated by systemic circulation. Each artery in _1_ receives a fraction of the total blood flow.

A

Parallel

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13
Q

When an artery is added in parallel, the total resistance _1_. In each parallel artery, the pressure is the _2_.

A
  1. decreases
  2. same
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14
Q

_1_ resistance is illustrated by the arrangement of blood vessels in a given organ. _2_ are the largest contributers to this resistance.

A
  1. Series
  2. Arterioles
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15
Q

As blood flows through the series of blood vessels, pressure _1_. Each blood vessel in series receives the _2_ total blood flow.

A
  1. decreases
  2. same
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16
Q

_1_ flow is streamlined. _2_ flow is not and causes audible vibrations called _3_.

A
  1. Laminar
  2. Turbulent
  3. bruits
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17
Q

A _1_ number predicts whether blood flow will be turbulent or laminar.

A

Reynold’s number

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18
Q

An increased Reynold’s number increases the likelihood of _1 (laminar/turbulent)_ flow.

A

turbulent

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19
Q

What are the two factors that increase a Reynold’s number?

A
  1. Decreased blood viscosity (ex. anemia, lower hematocrit)
  2. Increased blood velocity (ex. narrowing of a vessel [decreased radius)
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20
Q

What is hematocrit?

A

the volume percentage of red blood cells in blood

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21
Q

Pulse pressure is the difference between _1_ and _2_ presures.

A
  1. systolic
  2. diastolic
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22
Q

Aging leads to a _1_ in capacitacne and an _2_ in pulse pressure.

A
  1. decrease
  2. increase
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23
Q

When is systolic pressure measured?

A

**After **the heart contracts (systole) and blood is ejected in the **arterial **system.

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24
Q

When in diastolic pressure measured?

A

When the heart is relaxed (diastole) and blood is returned to the heart via the veins.

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25
Q

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.

A
  1. highest
  2. lowest
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26
Q

Mean arterial pressure = ?

A

MAP = 1/3 Systolic P + 2/3 Diastolic P

*because most of the cardiac cycle is spent in diastole

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27
Q

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.

A
  1. low
  2. high
  3. 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.

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28
Q

what are 4 methods of regulating arterial blood pressure?

A
  1. Increase pumping force
  2. contract veins and arterioles
  3. infuse fluids
  4. administer vasoconstrictors
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29
Q

which ventricle has a thicker muscular layer? why?

A

the left ventricle. It must pump blood through to aorta to systemic circulation.

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30
Q

how does the heart contract?

A

in a spiral contraction (like wringing a washcloth)

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31
Q

what is the % ejection volume referring to?

A

the amount of blood pushed out of the ventricles

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32
Q

capillaries have (high/low) velocity, (high/low) resistance and (high/low) cross-sectional area.

A

low

low

high

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33
Q

arterioles have the (highest/lowest) resistance

A

highest

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34
Q

the x descent on a jugular venous pulse reading is caused by what?

A

decrease in pressure in the right atrium (after peak of c wave after atrial relaxation)

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35
Q

what are the three types of action potentials? What differentiates the three?

A

atrial, ventricular, nodal

A/V have cardiac AP phases 0-4 while nodal only has 0, 3, amd 4

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36
Q

what does phase 4 represent in an atrial or ventricular cell?

In a nodal cell?

A

A/V: resting potential (constant horizontal line)

Nodal: pacemaler potential (not constant)

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37
Q

what does phase 0 represent in cardiac action potentials? what is the acting ion in a/v cells and nodal cells?

A

rapid depolarization and the start of an AP.

a/v: sodium Na+

nodal: Calcium Ca2+

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38
Q

phase 1 represents the brief, partial _1_ of ventricular and atrial action potentials. This phase is not present in _2_ APs.

A
  1. repolarization
  2. nodal
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39
Q

phase 2 looks different in every cell. It is a _1_ in ventricular cells, _2_ in atrial cells and _3_ in nodal cells.

A
  1. plateau
  2. abbreviated/shorter
  3. missing
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40
Q

what does phase 3 represent? How is the nodal cell different?

A

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)

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41
Q

what channel is responsible for the phase 4 resting potential?

A

the inwardly rectifying K+ channel that acts as if it is voltage-gated but is not.

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42
Q

what is the function of the ikr and iks channels?

A

they open during phase 2 and hekp the cell to repolarize back to resting level

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43
Q

what is a refractory period?

A

the point where initiation of a new action potential is difficult or impossible.

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44
Q

how does the ik1 inwardly rectifying channel allows a transition to phase 0?

A

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

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45
Q

what phases are included in the absolute refractory period? justify why.

A

Pjases 0-2. membrane depolarizes in 0 and the plateau ends by the end of 2

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46
Q

why is the supranormal refractory period associated with arrhythmias?

A

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.

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47
Q

a potassium channel (opens/closes) on depolarization and (opens/closes) on repolarization.

A

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)

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48
Q

what is the function of funny channels in phase 4 of the nodal action potential?

A

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.

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49
Q

what are the two calcium channels and their roles in the nodal action potential?

A

CaT opens during phase 4 to help depolarize the cell

CaL (long-lasting) is responsible for the big upstroke of the nodal action potential

50
Q

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?

A
  1. Ach
  • decreases (parasympathetic effects)
  • during pacemake potential: decreases Na+ and Ca2+ permeability and increases K+ permeability.
  • Hyperpolarizes the cell
51
Q

In nodal conductance, what is the effect of Ach on threshold?

A

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

52
Q

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.

A
  1. norepinephrine
  • increases sodium and calcium permeability, decreases potassium permeability.
  • depolarization
  • decreases
  • increases
53
Q

What are the connections for lead 1 on an EKG?

A

(-) right arm to (+) left arm

54
Q

What are the connections for lead 2 on an EKG?

A

(-) right arm to (+) left leg

(right leg is grounded)

55
Q

What are the connections for lead 3 on an EKG?

A

(-) left arm to (+) left leg

56
Q

what does the magnitude of the mean cardiac vector depend on?

A

the number of individual cells that are in the provess of depolarizing or repolarizing **and ** their orientation w/ respect to each other

57
Q

what is the mean cardiac vector for each case? (zero/non-zero)

  1. all cells at rest (repolarized)
  2. some cells de- and repolariz-ed/ing
  3. all cells contracted depolarized)
A
  1. zero
  2. non-zero
  3. zero
58
Q

whare are the three pacemaker nodes in the heart?

A

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.

59
Q

what is the Frank-Starling mechanism?

A

The strength required to contract the ventricles is proportional to the pressure of the end diastolic (filling) volume

60
Q

why does depolarization slow when going through the AV node?

A

allows the atria to completely empty into the ventricle

61
Q

What are the standard EKG leads? How many of each?

A

3 bipolar limb leads

3 unipolar limb leads

6 unipolar precordial chest leads

62
Q

why does R wave progression occur in readings of precordial chest leads?

A

the V1-6 is orientaed in the horizontal plane from the smaller right ventricle to the larger left ventricle.

63
Q

What differentiates on an EKG of V5-6 precordial chest leads?

A

They will show a Q wave on the EKG

64
Q

what does the PR interval indicate?

What can happen if it is prolonged?

A

the time it take for a signal to pass from the strium to the ventricle.

The signal can die out

65
Q

What is Wolff-Parkinson-White Syndrome

A

Where the PR interval is shortened and an extra delta wave is seen on an EKG. Could lead to supraventricular tachycardia

66
Q

what does a widened QRS indicated

A

slow electrical conduction through Purkinje Fibers and through the ventricular muscle.

67
Q

the QT interval represents what? Prolonged QT syndrome increases risk for what?

A

duration of ventricular action potential.

If prolonged, there is an increased risk for cardiac arrhythmia

68
Q

How are action potential and heart rate related?

A

a fast heart rate indicates a shorter action potental.

69
Q

the mean QRS is normal when there is an upward deflection in which leads?

A

lead I and II

70
Q

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

A

shorter, repolarize

71
Q

what does subendocardial ischemia look like on an EKG?

A

ST segment depression

*remember the endocardium is the first to depolarize therefore it will be that last to repolarize

72
Q

epicardial ischemia looks like what on an EKG?

A

ST segment elevation

73
Q

the left ventricle in the shape of a sphere indicate what pathogy?

A

heart failure

74
Q

the epicardium gets its blood supply from where?

A

the endocardium

75
Q

Calcium binds to _1_. _1_ moves tropomyosin from the _2_ site on the thin actin filament.

A
  1. troponin C
  2. binding
76
Q

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)

A
  1. sarcoplasmic
  2. reticulum
  3. extracellular
77
Q

Cardiac performance is determined by which four factors?

A
  1. Preload
  2. Afterload
  3. Contractility
  4. Heart Rate
78
Q

define preload? What is its significance? How is it measure?

A
  • 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
79
Q

define afterload.

how is it measured

should afterload increase or decrease during ejection?

A
  • 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.
80
Q

increasing preload (increases/decreases) the velocity and extend of shorteneing if afterload is constant.

Increasing afterload has the (same/opposite) effect.

A
  • preload increases velocity and shortening.
  • afterload has the opposite effect and is negatively correlated.
81
Q

when you have too much preload, the system backs up and can cause what?

A

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.

82
Q

what is the benefit of a stretched out sarcomere? What can cause sarcomeres to stretch?

A
  • it increases the calciumc binding sites on the sarcoplasm therefore increasing tension and strength of the contraction.
  • Increasing preload stretches sarcomeres.
83
Q

what is contractility? how is it regulated?

A

the strength of a contraction

beta adrenergic stimulation

84
Q

beta adrenergic receptors are regulated by what two things?

A
  1. the concentration of calcium
  2. the phosphorylation of proteins
85
Q

beta adrenergic receptors have what effect on the heart (3)?

A
  1. increase rate of contraction
  2. increase peak force
  3. increasing rate of relaxation
86
Q

what binds to the beta adrenergic receptor?

A

norepinephrine

87
Q

what four things can increase contractility?

A
  1. neural input (norepinephrine)
  2. increase catechols
  3. digoxin
  4. positive inotropic drugs (increase [Ca])
88
Q

what can reduce contractility (5)?

A
  1. acidosis (decrease oxygenated blood)
  2. ischemia (same as above)
  3. negative inotropic drug (decrease [Ca])
  4. calcium channel blockers
  5. beta-adrenergic blockers
89
Q

what is the equation for cardiac output?

A

CO=SV * HR

Cardiac output is equal to stroke volume multiplied b heart rate

90
Q

how would you increase preload in a patient?

A

give a patient IV fluids

91
Q

how are the semilunar and atriventricular valves opened?

A

high pressure in the ventricles and atria, respectively

92
Q

what is the difference in ventricular activity for diastole and systole?

A

diastole is ventricular filling (relaxation), systole is ventricular emptying (contraction)

93
Q

what is happening during the P wave?

A

atrial depolarization

94
Q

What is happening during the T wave?

A

ventricular repolarization until ventricular relaxation

95
Q

what is happening during the QRS complex?

A

ventricular depolarizaton to ventricular contraction

96
Q

what are the 5 stages of the left ventricular pressure-volume loop?

A
  1. isovolumetric contraction
  2. ejection (period between aortic valve opening and closing)
  3. isovolumetric relaxation
  4. rapid ventricular filling (as soon as mitral valve opens)
  5. slow ventricular filling (right before MV closes)
97
Q

what is happening in isovolumetric contraction?

A

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

98
Q

the period of rapid ejection begins when pressure within the ventricle is _1_ compared to the aorta or pulmonary artery?

A
  1. greater
99
Q

In isovolumetric relaxation, there is a _1_ in ventricular pressure.

It ends when there is what kind of relationship between the ventricle and atrium?

A
  1. decrease

when the pressure in the ventricle falls below the atrium

100
Q

What does the a wave represent in the atrium?

A

atrial contraction.

*follows P wave of EKG

101
Q

what does the c wave represent?

A

ventricular contraction

102
Q

what does the x descent represent (3)?

A
  1. ventricular emptying
  2. thoracic volume and pressure fall
  3. rapid fall in atrial pressure
103
Q

what does the v wave represent?

A

flow of blood from veins to atria.

*long period of time, AV valves are closed

104
Q

the v wave corresponds roughly with which segment of the EKG?

A

ST segment

105
Q

the *y *descent represents what?

A
  • atria draining into the ventricles
  • rapid fall in atrial pressure
106
Q

What does the S1 heart sound represent?

A

the mitral and tricuspid valves closing

*at this time the AoV and P valve are opening quietly

107
Q

What are you hearing with the S2 heart sound?

A

aortic and pulmonary valve closure

*as MV and TV valves open quietly

108
Q

What are you hearing with the S3 heart sound?

A

mitral regurgitation (preload is high, pressure in ventricle increases and MV opens as a result of increased pressure)

109
Q

what are you hearing with the S4 heart sound?

A

atrial contraction: the left atrium pushing against a stiff left ventricle

  • high atrial pressure
  • may lead to ventricular hypertrophy
110
Q

S4 occurs during with segment of the EKG? Which part of the jugular pulse curve?

A

P-Q interval; a wave (aortic contraction)

111
Q

S1 occurs during which part of the EKG diagram? jugular pulse?

A
  • QRS complex (mainly RS when isovolumentric contraction ends)
  • c wave (ventricular contraction)
112
Q

S2 occurs during what part of the EKG?

A

at the end of the T wave when the ventricle has finished emptying

113
Q

what is normal sinus rhythm?

A

a normal heart beat of 60-100 beats/minute

114
Q

while standing or sitting, aspirated material is most likely to go into which bronchus? which segment?

A

a right lower lobe basilar segment

115
Q

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

a widened QRS complex due to slow action potential conduction in the ventricular muscle

116
Q

for any given afterload, increasing preload usually has the effect of (increasing/decreasing) the velocity of muscle fiber shortening

A

increasing

117
Q

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”

A

“increased systolic calcium levels in the cytosol directly correlates with increased contractility”

118
Q

To determine the mean QRS, what leads are evaluated in an EKG?

A

Lead I and aVF

119
Q

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

A

D. 0 to -90 degrees

120
Q

If an aortic valve becomes stenotic, the peak systolic pressure would (increases/decreases) and the end systolic volume would (increase/decrease).

A

increase, increase

CPR-Week 1 (9 decks)

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