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Physiology I- Erin > Exam II > Flashcards

Exam II Flashcards

1
Q

What is a vector?

A

An arrow the points in the direction of the electrical potential generated by the current flow. Arrowhead points in positive direction. Length of the arrow is proportional to to the voltage of the potential.

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2
Q

In the ECG shown below, which of the following heart activities is represented?

a) sinus tachycardia
b) sinus bradycardia
c) complete AV block
d) incomplete second degree block with dropped beats

A

b

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3
Q

Which of the following conditions may result in tachycardia?

a) toxic conditions of the heart
b) increased body temp
c) sympathetic nerve stimulation
d) all of the above
e) B and C only

A

d

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4
Q

Circus movements are the basis of heart fibrillation. Which of the following statements is NOT true?

a) fibrillation may occur when the refractory period of the muscle is greatly shortened
b) fibrillation may occur when the pathway around the circle is too short
c) fibrillation may occur when the conduction velocity slows down
d) fibrillation may occur when the heart becomes dilated

A

b

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5
Q

What are the axes for the three leads on the ECG?

A

Lead I:
R= negative
L= positive
direction= 0 degrees

Lead II (right arm and left leg):
A= negative
L= positive
direction= 60 degrees
Lead III (left arm and left leg):
A= negative
L= positive
direction= 120 degrees
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6
Q

What will voltages be in accordance to the lead directions with the vector of the heart?

A
  • when vector of heart is perpendicular to axis of lead, the voltage recorded in the ECG is very low
  • heart vector has almost same axis as the axis of the lead, the entire voltage will be recorded
  • instantaneous mean vector: the summated vector of the generated potential at a particular instant
  • reference vector is horizontal and extends to left side
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7
Q

What is the vector of the heart in relation to the zero reference point?

A

59 degrees (mean electrical axis of the heart)

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8
Q

What is the vectorial analysis of the T wave?

A
  • the greatest portion of the ventricles to repolarize first is the outer surface near the apex
  • endocardial cells normally repolarize last
  • ventricular vector during repolarization is toward the apex of the heart
  • normal T wave in all three bipolar leads is POSITIVE
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9
Q

What is the vectorial analysis of the P wave?

A
  • atrial depolarization begins in the sinus node
  • vector direction is generally in the direction of the axes of the three limb leads
  • ECG is normally positive in all three leads
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10
Q

What is the vectorial analysis of the atrial T wave?

A
  • spread of depolarization through atrial muscle is slower than in ventricles
  • musculature around sinus node becomes depolarized a long time before the musculature in the distal parts of the atria
  • sinus node is the first to become repolarized
  • at the beginning of repolarization, the sinus node is positive with respect to the rest of the atria
  • obscured by QRS wave
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11
Q

What are the names of the leads utilized for an ECG?

A

six standard leads (V1-V6)

three augmented leads (aVR, aVL, aVF)

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12
Q

What can cause the heart’s axis to move?

A

ventricular conditions:

  • change in position of heart in the chest
  • hypertrophy of one ventricle
  • bundle branch block
  • fluid in pericardium
  • pulmonary emphysema
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13
Q

What can cause an increased voltage of the QRS wave in the bipolar leads?

A
  • occurs when the sum of the voltages of all the QRS complexes of the leads is greater than 4mV
  • most common cause is hypertrophy of the ventricle
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14
Q

What causes a decreased voltage of the QRS wave in a ECG?

A
  • caused by cardiac myopathies

- conditions surrounding the heart

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15
Q

With hypertrophy of the heart is the QRS shortened or lengthened? What can cause this abnormality?

A

lengthened from 0.06-0.08 to 0.09-0.12

Causes:

  • destruction of the cardiac muscle and replacement by scar tissue
  • multiple small local blocks in the conduction impulses at the many points in the Purkinje system
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16
Q

What characterizes a current of injury? The “trademark”

A
  • causes part of the heart to remain partially or totally depolarized all the time
  • current of injury flows between the pathologically depolarized and the normally polarized areas, even between heartbeats
  • the wave will begin above or below the J line due to the fact that the injured part is depolarized
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17
Q

What abnormalities cause an injury current?

A
  • mechanical trauma
  • infectious processes
  • ischemia (most common cause)
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18
Q

How does a current of injury affect the QRS wave?

A

-abnormal negative current flows from infarcted area and spreads toward the rest of the ventricles

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19
Q

What is the J point?

A

the reference point for analyzing current of injury

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20
Q

What is tachycardia and what are some causes?

A

-fast heart rate (greater than 100 bpm)

Causes:

  • increased body temperature (heart rate increase about 10bpF or 18bpC)
  • stimulation of the heart by sympathetic nerves (due to loss of blood and state of shock)
  • toxic conditions of the heart (results in weakening of the myocardium)
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21
Q

What is the difference between endogenously (exercise) and pathologically mediated tachycardia?

A

Endogenously:

  • heart rate increases and cardiac output increase
  • filling time is reduced but stroke volume does not fall
  • systolic interval is reduced allowing for more diastolic filling time
  • sympathetic and skeletal muscle pump increase venous return to help maintain ventricular filling

Pathological:

  • heart rate increases
  • cardiac output decreases
  • no muscle pump
  • mean atrial pressure decreases and activates the sympathetic nervous system, which occurs after the fact and is unable to compensate
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22
Q

What is bradycardia and what are some of the causes?

A

-slow heart rate (less than 60 beats/min)

Causes:

  • athletic heart
  • vagal stimulation
  • extremely sensitive carotid baroreceptors in carotid sinus syndrome
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23
Q

What is the respiratory type of sinus arrhythmia?

A

spillover signals:

  • from medullary respiratory center into vasomotor center during inspiratory and expiratory respiratory cycles
  • these signals alternately increase and decrease number of impulses transmitted through sympathetic and vagus nerves to the heart
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24
Q

What are the characteristics of a sinoatrial block?

A
  • sudden cessation of P waves
  • resultant standstill of atria
  • ventricles pick up a new rhythm, usually originating in the AV node
  • rate of QRS is slowed but not otherwise altered
  • no SA node, picks up AV node rhythm
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25
Q

What conditions cause an atrioventricular block?

A
  • ischemia of AV node or bundle fibers through coronary insufficient
  • compression of AV bundle by scar tissue or calcified portions of the heart
  • inflammation of the AV node or bundle
  • extreme stimulation of the heart by vagus
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26
Q

What are the characteristics of a first degree atrioventricular block?

A
  • normal P-R interval
  • increase in length with slower heartbeat and decreases with faster heartbeat
  • when P-R interval increases to greater than 0.20 seconds, the P-R interval is prolonged and patient has a first degree incomplete heart block
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27
Q

What are the characteristics of a second degree heart block?

A
  • P-R time interval increase to 0.25-0.45sec
  • atrial P wave is present but QRS-T wave may be missing, resulting in dropped beats of the ventricles
  • 2:1 rhythm or other variations may develop
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28
Q

What are some characteristics of a complete AV block?

A

-ventricles establish their own signal (usually AV node)
+if this ceases it takes ventricles 5-30secs to begin beating on their own (possibly due to Purkinje fibers acting as ectopic pacemaker = ventricular escape)
-no relation between the rate of the P waves and the rate of the QRS-T waves
-duration of block is variable (seconds to weeks)
-

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29
Q

What is Stokes-Adams syndrome?

A

after a complete block occurs, patients will often faint due to lack of blood to the brain until the ventricles escape, these fainting spells are Stokes-Adams sysndrome

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30
Q

What is a partial intraventricular block?

A
  • referred to as electrical alternans

- term refers to an alteration in the amplitude of P waves, QRS complexes, or T waves

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31
Q

What are some causes of premature contractions?

A

Anything that can interfere with the pathway between the SA node and Purkinje fibers:

  • local ischemic areas
  • calcified plaques
  • irritation of the conduction system or nodes
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32
Q

84% of the blood volume is in the systemic circulation. Of this, 64% is in which of the following vessels?

a) capillaries
b) systemic arterioles
c) veins
d) arterioles

A

c

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33
Q

Blood flow resistance is indirectly proportional to which of the following?

a) viscosity
b) vessel diameter
c) density
d) both a and c

A

b

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34
Q

Reynolds number is a measure of which of the following parameters?

a) tendency for turbulence
b) blood pressure
c) conductance
d) resistance

A

a

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35
Q

Which of the following represents the viscosity of blood with a hematocrit of 38-42?

a) 1.5
b) 3.0
c) 38
d) 42

A

b

1.5 is viscosity of plasma

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36
Q

What is a paroxysmal tachycardia?

A
  • heart rate increases suddenly and lasts for a few seconds, minutes, hours, or longer
  • they suddenly end and the pacemaker shifts back to the sinus node
  • can be either atrial or ventricular
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37
Q

What is fibrillation and what causes it?

A

Fibrillation- the twitching (typically slow) of the cardiac fibers in the atria or ventricles and recently denervated skeletal muscle fibers

-fibrillation is caused by the normal depolarization dying out in the heart muscle that has already contracted and is in the refractory period and cannot respond to being stimulated by the existing depolarization waves. This occurs due to circus movements.

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38
Q

What are the three different conditions that cause circus movements and explain them.

A
  1. the pathway around the circle is too long
    - due to dilated or hypertrophic heart
    - the impulse takes longer to get to the starting point and the muscle is no longer in the refractory period and can undergo another depolarization
  2. The length of the pathway remains the same, but the velocity slows down
    - usually occurs due to an ischemia, blockage of the Purkinje fibers, or excess K+ surrounding the heart
  3. the refractory period of the muscle might become greatly shortened
    - may occur in response to drugs such as epinephrine
    - may occur after repetitive electrical stimulation
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39
Q

What are some characteristics and causes of atrial fibrillation?

A
  • atrial muscle fibers are separated from the ventricular muscle fibers by the cardiac fibrous skeleton
  • ventricular and atrial fibrillation may occur separate from one another

Causes:

  • enlargement of the atria due to valve lesions (blood can travel back into the atria)
  • inadequate emptying of the ventricles causing blood to back up into atria
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40
Q

What are the differences between systemic and pulmonary bp?

A

systemic: 120/80
- drops to 0mm Hg by the time it reaches the termination of the vena cava
- systemic capillary pressure varies from 35mm Hg-10mm Hg

pulmonary: 25/8mm Hg

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41
Q

What is the overall blood distribution in the body?

A

84% systemic:

  • 64% veins
  • 13% arteries
  • 7% systemic arterioles and capillaries

16% in lungs and heart (pulmonary)

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42
Q

How do you calculate the velocity of blood flow? What is the velocity of the blood in the arteries and capillaries?

A

V=F/A, V=velocity, A=area, F=volume of blood flow

aorta: 33cm/sec at rest (area= 2.5cm2)
capillaries: 0.3mm/sec at rest (A= 25000cm2)

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43
Q

What are the functional principles of the circulatory system?

A
  1. rate of blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue need.
  2. the cardiac output is controlled mainly by the sum of all the local tissue flows.
  3. arterial pressure is generally independent of either local blood flow control or cardiac output control
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44
Q

How is tissue blood need monitored?

A

-microvessels

+monitors O2, CO2, and wastes and then acts directly on local blood vessels and dilate or constrict accordingly

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45
Q

How does the heart respond to tissue needs?

A

-nerve signals may be needed to help regulate heart rate, but the heart responds to the demands of the tissues

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46
Q

How is arterial pressure regulation independent?

A

-if arterial pressure falls below 100mm Hg, nervous reflexes:
+increase force of heart pumping
+constrict large venous reservoirs
+generally constrict most of the arterioles throughout the body (increase pressure_
+kidneys may later play important role in pressure control

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47
Q

What two factors affect blood flow? What is the equation that can be used to explain this?

A

-pressure and resistance

-Pouiseille’s law:
F = (delta)P/R, measured in mL/min or L/min

-adult at rest -> 5000mL/min

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48
Q

The least amount of damping of the pressure pulses would occur in which of the following components of the circulatory system?

a) femoral artery
b) arterioles
c) capillaries
d) venules

A

a

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49
Q

Which of the following factors affect(s) pulse pressure?

a) vascular elastance
b) arterial compliance
c) stroke volume
d) all of the above
e) b and c only

A

e

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50
Q

Which of the following is the most important means for the exchange of substances between the blood and the interstitial fluid?

a) blood hydrostatic pressure
b) capillary oncotic pressure
c) diffusion
d) interstitial fluid hydrostatic pressure
e) osmosis

A

c

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51
Q

What is laminar flow and what are some characteristics of laminar flow?

A

-streamline flow
-blood flows at a steady rate
-blood vessel is long and smooth
-blood flows in layers
+each layer maintains same distance from vessel wall
+central-most portion of the blood stays in the center
+each layer slips easily past surrounding layers
+velocity of fluid flowing in center is greater than that of fluid flowing towards the outer edge

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52
Q

What is turbulent flow and some characteristics of it?

A

-turbulent flow is non-layered flow
-creates murmurs
-produces more resistance than laminar flow
-occurs when:
+flow is too great great
+blood passes an obstruction within the vessel
+blood has to make a sharp turn
+blood passes over a rough surface
-blood flows with greater resistance when eddy currents flow (swirling flow)

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53
Q

What factors influence turbulent flow?

A
  • in direct proportion to velocity of blood flow
  • in direct proportion to the diameter of the vessel
  • in direct proportion to the density of the blood
  • inversely proportional to the viscosity of the blood
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54
Q

How does viscosity and density affect blood flow?

A
  • blood is denser than water, specific gravity 1.055
  • blood density depends on the proportion of its components and in particular of RBCs and proteins
  • blood is more vicous than water
  • viscosity is 4.5
  • blood viscosity is the property of blood to adhere to the vessel walls and to each other based on size, shape, and number
  • viscosity ensures laminar flow (in layers) of blood through the vessels
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55
Q

What is a Reynolds number?

A

-measure of the tendency for turbulence to occur

Re= vd p/ n

v=velocity
d= vessel diameter (cm)
p= density
n= viscosity (in poise), normally 1/30 poise

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56
Q

What are typical Reynolds number?

A
  • when Re rises above 200-400, turbulent flow will occur in some regions of a vessel
  • when Re rises above 2000, turbulence will occur even in a straight vessel
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57
Q

What is blood pressure?

A

-the force exerted by the blood against any unit area of the vessel wall. Measured via sphygmomanometer or electronic transducers

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58
Q

What is resistance?

A
  • impediment to blood flow in a vessel

- indirectly calculated from measurements of blood flow and pressure (peripheral resistance unit)

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59
Q

What factors influence resistance?

A
  • vessel radius (most important)
  • blood viscosity
  • vessel length

increased resistance: decreased blood flow, upstream pressure increased, downstream pressure decreased

rate of blood flow through entire circulatory system:
=100mL/sec
pressure difference from systemic arteries to systemic veins
=100mm Hg
resistance of entire systemic circulation
=100/100= 1PRU

  • in conditions where vessels are strongly constricted, total peripheral resistance may rise to 4PRU -> sympathetic
  • when vessels are dilated, the resistance can fall to as little as 0.4PRU

-pulmonary vascular resistance= 0.14PRU

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60
Q

What is conductance?

A

-the measure of blood flow through a vessel for a given pressure difference
+expressed in mL/sec per mL Hg
-reciprocal of resistance and directly proportional to diameter^4
-a fourfold increase in vessel diameter can increase the flow by as much as 256x -> minor changes in arteriole diameter greatly increases blood flow

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61
Q

What is the equation for conductance?

A

F= (pi)(deltaP)r^4/8nl

F= rate of blood flow (mL/min)
delta P= pressure difference between ends of vessel
r= radius of vessel
l= vessel length
n= blood viscosity
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62
Q

How is blood flow affected when there are vessels arranged in parallel series?

A

-total resistance of blood flow is expressed as:
1/Rtotal = 1/R1 + 1/R2 + etc
the resistance of a parallel series is less than a single blood vessel
-total conductance for vessels arranged in parallel is the sum of the conductance of each parallel pathway

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63
Q

What systems are arranged in parallel and how are the systems affected when a parallel circuit is removed?

A
  • brain
  • kidney
  • muscle
  • GI
  • skin
  • coronary circulation
amputation or removal of a kidney (for example)
removes a parallel circuit:
-reduces total vascular conductance
-reduces total blood flow
-increases total vascular resistance
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64
Q

What is the relationship between resistance and viscosity?

A

-viscosity is a measure of the fluid’s internal resistance
-the greater the viscosity, the greater the resistance
-prime determinant of blood viscosity is hematocrit
-blood is 3x more viscous than water
+hematocrit men: 42, women: 38
+normal viscosity: 3
+when hematocrit rises to 60-70 (polycythemia), viscosity= 10
+viscosity of blood plasma w/o RBCs = 1.5, same as water
-anemia decreases viscosity

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65
Q

When does autoregulation occur? (parameters)

A

75-175mm Hg

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66
Q

What is vascular distensibility?

A

increase in volume/ increase in pressure * original volume

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67
Q

Compare the distensibility between arteries and veins.

A
  • veins are 8x more distensible than arteries
  • pulmonary vein distensibility is about the same as the systemic veins
  • pulmonary artery distensibility is about 6x that of systemic arteries
  • the more pressure needed to increase volume, the less distensible the vessel is
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68
Q

What is vascular compliance/capacitance?

A

-total quantity of blood that can be stored in a given portion of the circulatory system

increase in volume/ increase in pressure

-describes distensibility of blood vessels
-tells us the quantity of blood (mL() that can be stored in a given portion of the circulation for each mm Hg rise in pressure
-inversely proportional to elastance
+elasticity of arteries decreases with age

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69
Q

What is elastance?

A

-a measure of the tendency of a hollow viscus to recoil toward its original dimensions upon removal of a distending or collapsing force

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70
Q

What is pulse pressure? What factors affect it?

A

stroke volume/arterial compliance

  • most important determinant of pulse pressure
  • diastolic pressure remains unchanged during ventricular systole, pulse pressue increases to the same extent as the systolic pressue
  • decreases in compliance result in increase in pulse pressure
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71
Q

What conditions cause abnormal contours in the pulse pressure wave?

A
  1. Aortic valve stenosis:
    - diameter of the aortic valve opening is reduced significantly and the aortic pressure pulse is decreased significantly
    - blood flow through the aortic valve is diminished
  2. Atherosclerosis
  3. Patent ductus arteriosus:
    - half or more of the cardiac output flows back into the pulmonary artery and lung blood vessels
    - diastolic pressure falls very low before next heartbeat
  4. Aortic regurgitation:
    - the aortic valve is absent or will not close completely
    - aortic pressure may fall to 0 between heartbeats
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72
Q

On the pressure pulse contour what is the incisura indicative of?

A

-the aortic valve closing

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73
Q

What is damping and what does it apply to?

A
  • applies to pulse pressure

- the progressive reduction of the pulsations in the periphery

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74
Q

How is arterial pressure measured and what do the sounds mean?

A
  • sphygmomanometer on brachial artery

- Korotkoff sounds are the first sound and last sound -> turbulent

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75
Q

Where does mean blood pressure lie compared to systole and diastole? Why is it positioned as such?

A

The mean bp lies in between systole and diastole, but closer to diastole. This is because 60% of the cardiac cycle is spent in diastole and 40% in systole.

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76
Q

What is the calculation for mean arterial pressure?

A

diastolic pressure + 1/3 pulse pressure

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77
Q

What is the pressure in the right atrium called? What are some factors that regulate it?

A

central venous pressure

  • ability of the heart to pump blood out of the right atrium/ventricle
  • tendency of blood to flow into the right atrium
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78
Q

What are some factors that increase venous return and increase rt atrial pressure?

A
  • increased blood volume
  • increased peripheral venous pressures due to increased large vessel tone
  • dilation of arterioles
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79
Q

How does resistance change with body position?

A
  • in a person lying down the pressure in the peripheral veins is +4 to +6 mm Hg greater than the right atrial pressure
  • when intra-abdominal pressure increases, the venous pressure in the legs must increase above the abdominal pressure before the blood can flow from the legs to the heart through the abdominal veins
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80
Q

How does intro-thoracic pressure influence venous return?

A
  • negative intro-thoracic pressure encourages venous return

- positive is the opposite

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81
Q

How does gravity affect venous return?

A
  • anything above the heart is generally negative to 0

- anything below the heart is positive, so muscle pumps are critical to getting the blood back

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82
Q

How does altering blood volume affect pressure?

A

-the body will attempt to “equalize” it

+decrease the pressure with an increase in blood and increase pressure with a decrease in blood

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83
Q

What are varicose veins?

A

-valves in veins, typically in legs, collapses and blood pools. This causes a protrusion in the vein.

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84
Q

How do arterioles influence blood flow?

A

-small arterioles control blood flow to each tissue
-local conditions in tissues control diameters of arterioles
-arterioles are highly muscular
+continuous muscular coat is lost in metarterioles

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85
Q

What is a pre-capillary sphincter?

A

smooth muscle fiber that encircles capillary at point where it originates from a metarteriole

86
Q

What are some characteristics of a capillary wall?

A
  • unicellular layer of endothelial cells
  • thin basement membrane
  • total wall thickness= 0.5 micro
  • internal capillary diameter= 4-9 micro, blood is 7
87
Q

What are the three modes of transportation to and from a capillary?

A

slit pores: intercellular clefts spacing 607nm
-allow for rapid diffusion of water, water soluble ions and small solutes
plasmalemmal vesicles:
-formed from caveolins (similar to clatherin)
-play a role in endocytosis and transcytosis
pores:
-in liver, GI tract, kidneys

88
Q

What is the most important factor in regulating vasomotion?

A

concentration of oxygen in the tissues

89
Q

What can and can’t diffuse through a capillary?

A
  • fat soluble substances can diffuse through a capillary -> oxygen and CO2
  • non-lipid soluble substances diffuse through the intercellular pores/clefts
  • rate of water diffusion through the capillary membrane is 80x faster than flow of plasma within the capillary
90
Q

Why is passage of substances through capillaries primarily through diffusion rather than flow?

A
  • due to large numbers of proteoglycan filaments found in the interstitium
  • rivulets that allow fluid flow through the interstitium do sometimes flow
91
Q

What are the inward and outward forces acting on a capillary?

A

Inward

  • interstitial fluid pressure
  • capillary plasma colloid osmotic pressure

Outward

  • capillary pressure
  • interstitial fluid colloid osmotic pressure
92
Q

What net filtration process equation?

A

NFP= Pc -Pif - (pi)p + (pi)if

Pc= capillary pressure (outward)
Pif= interstitial fluid pressure (inward)
(pi)p= plasma colloid osmotic(oncotic) pressure (inward)
(pi)if= interstitial colloid osmotic (oncotic) pressure (outward)
93
Q

What is the capillary filtration coefficient?

A

Kf -> takes into consideration the number and size of pores
filtration= NFP * Kf

-when fluid enters the lymphatics, the lymph vessel walls contract momentarily and pump fluid into the blood circulation
+creates a slight negative pressure in the interstitial spaces

94
Q

How is lymph returned?

A

rate of lymph flow = interstitial fluid pressure * activity of lymphatic pump

  • lymph vessel possess 1 way valves
  • lymph flow reaches max when interstitial pressure roses slightly above atmospheric pressure
95
Q

What are factors that increase lymph flow?

A
  • elevated capillary hydrostatic pressure
  • decreased plasma colloid osmotic pressure
  • increased interstitial fluid colloid osmotic pressure
  • increased permeability of capillaries
96
Q

Why do lymph nodes swell?

A

-contain a lot of macrophages, T cells, B cells and when an infection is detected these proliferate

97
Q

How does the body control blood flow short term and long term?

A

acute:
- rapid changes in local vasodilation/vasoconstriction
- occurs in seconds to minutes
- basic theories (vasodilator theory, oxygen/ nutrient lack theory)

long term control:

  • increase in sizes/number of vessels
  • occurs over a period of days, weeks, months
98
Q

What does the vasodilator theory state?

A

increase in metabolism -> decrease oxygen availability -> formation of vasodilators

(adenosine, CO2, adenosine phosphate compounds, histamine, K+, H+)

99
Q

What does oxygen/nutrient lack theory state?

A

decrese oxygen conc -> blood vessel relaxation -> vasodilation

-muscles relax and vessels can dilate

100
Q

What is the definition of vasomotion?

A
  • cyclical opening and closing of pre capillary sphincters
  • # of pre capillary sphincters open at given time is roughly proportional to nutritional requirements of tissue. The assumption is that smooth muscles require oxygen to remain contracted
101
Q

What is the difference between active and reactive hyperemia?

A

active: when any tissue becomes active, rate of blood flow increases
reactive: a tissue has its blood supply cut off and when it becomes unblocked blood flow increases 4-7x above normal

102
Q

What is autoregulation?

A
  • in any tissue rapid increase in arterial pressure leads to increased blood flow
  • within minutes, blood flow returns to normal even with elevated pressure
103
Q

What are the two theories of autoregulation and what do they state?

A

metabolic theory:
-increase in blood flow -> too much oxygen and nutrients -> washes out vasodilators

myogenic theory:
-stretching of vessels -> reactive vasculature constriction

104
Q

What parts of the body utilize acute blood flow regulations?

A
  • kidneys: tubuloglomerular feedback -> macula densa and juxtaglomerular apparaus
  • brain: increased conc CO2 and H+ -> cerebral vessel dilation -> washing out of excess CO2/H+
  • skin: blood flow linked to body temp, sympathetic nerves via CNS, 3mL/min/100g tissue (7-8L/min for entire body)
105
Q

What are the endothelial mechanisms for blood flow for undamaged and damaged cells?

A

healthy cells -> NO -> cGTP -> cGMP -> activation protein kinase -> vasodilation

damaged cells (hypertension) -> endothelin -> vasoconstriction
*inhibits NO
106
Q

What hormones control blood flow?

A

vasoconstriction:

  • norepinephrine
  • epinephrine
  • angiotensin II
  • vasopressin (ADH)

vasodilation:

  • bradykinin (increase capillary permeability)
  • histamine (derived from mast cells and basophils)
107
Q

What are the vasomotor areas in the brain and what do they do?

A

vasoconstrictor area:
-anterolateral portions of upper medulla
-transmits continuous signals to blood vessels
+continual firing results in sympathetic vasoconstrictor tone
+partial state of contraction of blood vessels = vasomotor tone
vasodilator area:
-bilateral in the anterolateral portions of lower medulla
-inhibits activity in vasoconstrictor area
sensory area:
-bilateral in tractus solitarius in postolateral portion of medulla
-receives signals via (vagus and glossopharyngeal)
reticular substance (RAS)
hypothalamus
cerebral cortex

108
Q

What does the adrenal medulla do?

A

secretes epinephrine and norepinephrine

109
Q

When does the vasomotor center alter the blood flow?

A

-simultaneous changes
+constriction of most systemic arteries
+constriction of veins
+increased heart rate
-rapid response (within secs_
-increased bp during exercise (accompanied by vasodilation)
-alarm reaction (fight or flight)

110
Q

Where are the baroreceptors located?

A

-aortic arch and carotid sinus

111
Q

What is stimulated by low pressure?

A
  • carotid sinuses are stimulated by pressure greater than 60mm Hg
  • aortic sinus is stimulated by pressure greater than 30mm Hg
  • vagus nerve
  • glossopharyngeal nerves via small Herring’s nerves (carotid)
112
Q

What are the signals that the baroreceptors send?

A
  • inhibit vasoconstrictor center
  • excite vasodilator center
  • signals cause either increase or decrease in arterial pressure
  • primary function is to reduce the minute-by-minute variation in arterial pressure
113
Q

What are chemoreceptors?

A
  • located in carotid bodies in bifurcation of the common carotids and in aortic bodies
  • chemosensitive cells sensitive to lack of oxygen, carbon dioxide excess, and hydrogen ion excess
  • signals pass through Herring’s nerves and vagus nerve
  • play a more important role in respiratory control
114
Q

What are the atrial reflexes?

A

-low pressure receptors are located in the atria and pulmonary arteries and play an important role in minimizing arterial pressure changes in response to changes in blood volume

115
Q

What does an increase in atrial stretch result in?

A
  • reflex dilation of kidney afferent arterioles (increase kidney fluid loss, decreased blood volume)
  • increase in HR
  • signals to hypothalamus -> decreases in ADH
  • atrial natriuretic peptide (ANP) -> kidneys (increase GFR, decrease Na+ reabsorption)
  • decrease Na+ reabsorption
116
Q

How is arterial pressure calculated?

A

arterial pressure = cardiac output * total peripheral resistance
-normal functioning kidneys return the arterial pressure back to normal within a day or two due to pressure diuresis and pressure natriuresis

117
Q

What are the characteristics of hypertension?

A
  • increased cardiac output
  • increased sympathetic nerve activity
  • increase in angiotensin II and aldosterone levels
  • impairment of renal-pressure natriuresis mechanism
  • inadequate secretion of salt and water
118
Q

What is primary hypertension?

A

-hypertension of unknown origin (90-95%)
-major factors:
+weight gain, characterized by increased cardiac output, increased sympathetic nerve activity, increased angiotensin II and aldosterone levels, impaired renal-pressure natriuresis mechanism
+sedentary life style

119
Q

What is secondary hypertension?

A 
-hypertension second to some other cause
   \+tumor affecting renin-secreting juxtaglomerular cells
   \+renal artery constriction
   \+coarctation of the aorta
   \+preeclampsia
   \+neurogenic hypertension
   \+genetic causes
120
Q

What some renal causes of hypertension?

A
  • chronic renal disease
  • renal artery stenosis
  • renin-producing tumors
  • acute glomerulonephritis
  • polycystic disease
  • renal vasculitis
121
Q

What are some endocrine reasons for hypertension?

A
  • Cushing’s disease (adrenocortical hyperfunction)
  • exogenous hormones (gluticorticoids, estrogen)
  • pheochromocytoma
  • acromegaly
  • hypothyroidism
  • hyperthyroidism
  • pregnancy
122
Q

What are some cardiovascular causes of hypertension?

A
  • coarctation of the arteritis nodosa
  • increased intravascular volume
  • rigidity of the aorta
  • increased cardiac output
123
Q

What are some neurologic causes of hypertension?

A
  • psychogenic
  • increased intracranial pressure
  • sleep apnea
  • acute stress
124
Q

What are some contributing factors for hypertension?

A
  • genetic factors
  • other single gene disorders that alter sodium reabsorption by the kidneys
  • genetic variants in the renin-angiotensin system
  • stress
  • obesity
  • smoking
  • physical inactivity
  • heavy consumption of salt
125
Q

What are some factors resulting in decreased peripheral resistance leading to decreased bp? What increases it?

A
  • increased production of NO
  • increased release of prostacyclin
  • increased release of kinins
  • increase in ANP
  • decreased neural factors (beta adrenergic)

Increases:

  • increased angiotensin II
  • increased catecholamines (epi and NE)
  • increased thromboxane
  • increase neural factors (alpha adrenergic)
126
Q

What factors decreased cardiac output thus decreasing blood pressure? What increases it?

A
  • decreased blood volume
  • decreased heart rate
  • decreased contractility

Increase:

  • increased heart rate
  • increased contraction
  • increased blood volume (aldosterone)
127
Q

What are vasodilators and vasoconstrictors?

A

Vasodilators:

  • kinins
  • prostaglandins
  • NO

Vasoconstrictors:

  • angiotensin II
  • catecholamines
  • endothelin
128
Q

What are some lethal effects of chronic hypertension?

A
  • early heart failure and coronary heart disease
  • cerebral infarct
  • kidney failure
129
Q

What are the non-modifiable risk factors for atherosclerosis?

A
  • age (increase with age, most around age 40-60 and increases with each decade)
  • gender (increases in men and post menopausal women)
  • genetics
130
Q

What are the modifiable factors for atherosclerosis?

A
  • hyperlipidemia (correlated with high levels of LDL as opposed to HDL)
  • hypertension
  • cigarette smoking
  • diabetes
131
Q

What are other risk factors for atherosclerosis?

A
  • inflammation
  • hyperhomocystinemia (inborn metabolic error, premature vascular disease)
  • metabolic syndrome (associated with insulin resistance -> obesity, fasting hyperglycemia, increased lipid triglycerides, decreased HDL, hypertension)
  • lipoprotein a
  • factors affecting hemostasis
  • sedentary lifestyle
132
Q

How does endothelial tissue injury result in atherosclerosis?

A
  • results in intimal thickening
  • may lead to formation of atheroma in presence of hyperlipidemia
  • factors related to endothelial dysfunction:
\+hypertension
\+hyperlipidemia
\+cigarette smoke
\+infectious agents
\+homocysteine
\+hemodynamic disturbances
\+hypercholesterolemia
133
Q

How is an atherosclerotic plaque created?

A

-accumulation of lipoproteins (LDL)
+accumulate in intima and are oxidized by free radicals generated by macrophages or endothelial cells
+oxidized LDL is ingested by macrophages which become foam cells
+oxidized LDL stimulates release of growth factors, cytokines, and chemokines
+oxidized LDL is toxic to endothelial cells and smooth muscle
-monocyte adhesion to endothelium
+express VCAM-1 adhesion molecules that bind monocytes and T cells to endothelium
+monocytes transform into macrophages and engulf lipoproteins
+T cells stimulate a chronic inflammatory response
+activated leukocytes and endothelial cells release growth factors that cause smooth muscle to proliferate
-smooth muscle proliferates
+fatty streak into a mature atheroma

134
Q

What is the morphology of an atheroma?

A

-cap of smooth muscle cells, macrophages, foam cells (converted macrophages) and other extracellular components, overlying necrotic center composed of cell debris, cholesterol, foam cells, and calcium

135
Q

What are the developmental stages of an atheroma?

A
  • earliest lesion s are fatty streaks
  • plaques impinge on the lumen of the artery and grossly appear white or yellow
  • plaques enlarge due to cell death and degeneration and synthesis/degradation of extracellular matrix
  • undergo calcification
  • plaques may rupture, ulcerate, or erode
136
Q

What are the common sites for atheromas?

A
  • lower abdominal aorta
  • coronary arteries
  • popliteal arteries
  • internal carotid arteries
  • circle of Willis
137
Q

What happens as arterial pressure increases?

A

-increase in urine output (pressure diuresis) and sodium output (pressure natriuresis)

138
Q

What are the primary determinants of the long term arterial pressure?

A
  • degree of pressure shift of the renal output curve for water/salt
  • lve; pf water/salt intake
139
Q

What are chronic hypertension?

A

-one’s mean arterial pressure is greater than the upper range of the accepted normal measure

normal: 90mm Hg (100/70)
hypertensive: 110mm Hg (135/90)
severe hypertensive: 150-170mm Hg (250/130)

140
Q

What are the lethal effects of chronic hypertension?

A
  • early heart failure
  • coronary heart disease
  • heart attack
  • cerebral infarct
  • destruction of areas of kidneys -> kidney failure -> uremia -> death
141
Q

Describe the renin-angiotensin system.

A

decreased bp -> kidney secrets renin -> renin converts angiotensinogen to angiotensin I -> angiotensin I is converted into angiotensin II from ACE (lungs) ->angiotensin II increases bp -> volume overload in heart -> ANP -> vasodilation

angiotensin II -> adrenal gland -> aldosterone -> kidney -> sodium and water reabsorption

142
Q

What is Goldblatt hypertension?

A

-occurs when one kidney is removed and remaining renal artery is constricted

143
Q

Define cardiac output.

A
  • quantity of blood pumped into the aorta each minute by the heart
  • quantity of blood that flows through the circulation
  • sum of all the blood flows to all the tissues of the body
144
Q

Define cardiac index.

A

cardiac output per square meter of body surface

145
Q

How do you calculate cardiac index and what is normal?

A

cardiac index = cardiac output/ body SA

Normal: 3L/min/m2

146
Q

How is cardiac index affected as you age?

A

-it peaks around the age of ten and then continually decreases due to increasing SA and decreasing muscle mass and activity level (metabolism)

147
Q

What is the Flick Principle of blood flow?

A

-used to calculate blood flow through an organ

cardiac output = O2 consumption/ [O2] pul veins - [O2] pul art

148
Q

What are the determining factors that control how much blood the heart pumps out?

A

-heart is a “demand” organ, pumps out whatever blood is returned via venous system -> amount of blood returning to heart affects amount pumped out

149
Q

What are the similarities and differences between and systemic and pulmonary blood flow?

A
  • two are connected in series:
  • flow must be equal in the two circuits
  • cardiac output and rate of the two circuits are equal
  • all pressures are higher in the systemic circuit
  • chemical composition of pulmonary venous blood is similar to that of systemic arterial blood
150
Q

What are the factors that affect cardiac output? (amount of blood flow into heart)

A
  • metabolism
  • whether person is exercising
  • age
  • size of body

-5L/min is normal for resting adult

151
Q

What are the principles that govern cardiac output?

A
  • Frank-Starling law -> stretch of heart
  • Bainbridge reflex
  • under non-stressful conditions the CO is controlled by peripheral factors that determine venous return
  • Ohm’s Law: long term level of total peripheral resistance changes the cardiac output changes quantitatively in exactly the opposite direction
152
Q

What is the Bainbridge reflex?

A

-atrial stretch reflex, responds in changes to blood volume as detected by receptors in the RA
-contrast with baroreceptors which respond to arterial pressure
+significant in humans ONLY after birth when the uteroplacental blood returns to the mother’s circulation and results in tachycardia

153
Q

What factors contribute to a hypereffective heart?

A

-nervous stimulation
-hypertrophy of the heart
-exercise via the nervous system
+increase in metabolism causes arterioles to relax -> more blood in arterioles -> brain sends motor signals to the muscles and ANS to excite circulatory activity -> causes vein constriction -> increased HR and contractility

154
Q

What factors contribute to a hypoeffective heart?

A
  • increased arterial pressure (hypertension)
  • inhibition of nervous excitation of the heart
  • pathological factors causing abnormal heart rhythm/rate
  • coronary artery blockage
  • valvular heart disease
  • congenital heart disease
  • cardiac hypoxia
155
Q

What factors cause decreasing cardiac output?

A
  • severe blood vessel blockage -> myocardial infarction
  • severe valvular disease
  • myocarditis
  • cardiac tamponade
  • cardiac metabolic arrangements
156
Q

What are the non-cardiac reasons for decreased cardiac output?

A
  • decreased blood volume
  • acute venous dilation
  • obstruction of large veins
  • decreased tissue mass (muscle)
  • decreased metabolic rate of tissues
157
Q

What is the mean systemic filling pressure of the RA?

A

+7mm Hg

-at -2mm Hg venous return reaches a plateau -> caused by collapse of veins entering chest

158
Q

What is the mean systemic filling pressure?

A
  • 0 when blood volume is 4L
  • 7 mm Hg when blood volume is 5L
  • almost equal to mean systemic filling pressure
159
Q

What systemic circulation factors affects venous return?

A
  • the greater the difference between the mean systemic filling pressure and the Ra pressure, the greater the venous return
  • the difference between the mean systemic filling pressure and the RA pressure -> pressure gradient for venous return
160
Q

How does resistance affect venous return?

A
  • about 2/3 of the resistance to venous return is determined by venous resistance (vein distensibility, there is little rise in venous ressure)
  • aboiut 1/3 of the resistance to venous return is determined by arteriolar and small artery resistance (accumulation of blood overcomes resistance)
161
Q

What is an equation characterizing resistance and venous return? What is the pressure gradient eqn?

A

venous return = mean systemic filling pressure -RA pressure/ resistance to venous return

-top is pressure gradient

162
Q

Factors affecting venous return.

A
  • right atrial pressure
  • mean systemic filling pressure
  • blood flow resistance between peripheral vessels and RA
163
Q

How are venous return and right atrial pressure related?

A

inversely, VR is high, RAP is low

164
Q

Why does beriberi result in increased cardiac output?

A

-decreasing peripheral resistance

165
Q

How does sympathetic stimulation and inhibition affect mean circulatory filling pressure?

A

sympathetic stimulation = smaller volume than normal, venous return increases, increasing RA pressure, less resistance

sympathetic inhibition = larger volume than normal, but venous return decreases, decreasing RA pressure, more resistance

166
Q

What increases peripheral systemic filling pressure?

A
  • increase vascular volume -> infusion or activation of renal-angiotensin-aldosterone system
  • decrease venous compliance -> sympathetic stimulation, muscle pump, exercise, lying down
167
Q

What does increasing Psf result in?

A
  • shift in vascular return curve to the right

- enhances filling of the ventricles

168
Q

Decrease in Psf and result?

A
  • decrease vascular volume (hemorrhage, burn trauma, vomiting, diarrhea
  • increase venous compliance (inhibits sympathetics, alpha block, venodilators, standing upright

Results in:

  • shift in vadular return curve to the left
  • reduces filling of the ventricles
169
Q

How is blood flow regulated to the skeletal muscle?

A 
-due to chemicals that act directly on them due to:
   \+reduction on oxygen
   \+adenosine
   \+potassium ion
   \+ATP
   \+lactic acid
   \+CO2
170
Q

What are the nervous controls to regulate blood flow?

A 
-sympathetic vasoconstrictor nerves:
   \+secrete NE
   \+can decrease blood flow through resting muscle to as little as 1/2 to 1/3 normal
-adrenal medulla
   \+secrete NE and epi
   \+epi has a slight dilator effect
171
Q

What mechanisms increase blood flow during exercise?

A

-heart rate increases
-peripheral arteries are strongly contracted except those in active muscles, coronary arteries, and cerebral arteries
-muscle walls of veins are contracted -> increase msfp
-increase in arterial pressure
-sympathetic stimulation causes:
+vasoconstriction of arterioles and small arteries
+increased pumping of heart
+increase mean filling pressure caused by venous contraction

172
Q

How does blood flow to a calf muscle during exercise?

A

-blood flow decreases during contraction and increases between contractions

173
Q

How is coronary blood flow affected during a heart cycle?

A

Systole:
-coronary blood flow in the left ventricle falls to a low value (opposite flow in vascular beds elsewhere in the body)
Diastole:
-cardiac muscle relaxes and no longer obstructs blood flow through the left ventricular capillaries

174
Q

What factors affect coronary blood flow?

A
  • muscle metabolism (MOST IMPORTANT)
  • coronary flow increases in direct proportion to additional metabolic consumption of oxygen by heart -> vasodilaters?
  • direct ANS stimulation
  • indirect ANS stimulation is on cardiac muscle tissue and indirectly on the coronary vessels via local control mechanisms
175
Q

What are some causes of death after a coronary occlusion?

A
  • decreased cardiac output
  • damming of blood in pulmonary blood vessels and death resulting from pulmonary edema
  • fibrillation of heart
  • rupture of heart
176
Q

Define cardiac failure.

A

failure of the heart to pump enough blood to satisfy the needs of the body

177
Q

How does the body try to compensate for acute cardiac failure?

A

-sympathetic stimulation increased
+strengthen contraction
+increases tone of vessels, especially veins (increases mean systemic filling pressure)

178
Q

How does the ANS compensate for acute cardiac failure?

A
  • barorecptor reflex
  • chemorector reflex
  • CNS ischemic response
179
Q

How is the blood flow changed after acute heart attack?

A
  • reduced cardiac output
  • damming of blood in the veins -> increased venous pressure
  • compensated by sympathetics
180
Q

How does the heart compensate after heart failure?

A
  • result for partial heart recovery and renal retention of fluid
  • max pumping ability of the partly recovered heart is still depressed to less than one half normal
  • any attempt to perform heavy exercise usually results in immediate return of symptoms of acute failure because heart can’t increase pumping capacity
  • increase in RA pressure can maintain cardiac output despite weakness of heart
181
Q

What are the two major problems of left heart failure? Why does this happen?

A
  • pulmonary vascular congestion
  • pulmonary edema (can occur in death by suffocation in 20-30 mins)
  • left side of the heart fails without concomitant failure of the right side
  • blood continues to be pumped into the lungs, but it is not pumped adequately out of the lungs
  • the mean pulmonary filling pressure rises because of the shift of large volumes of blood from the systemic circulation into the pulmonary circulation
  • pulmonary capillary pressure increase
  • if this rises above a value equal to the colloid osmotic pressure of the plasma (28mm Hg) fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli, resulting in pulmonary edema
182
Q

How does digitalis work on a chronically failing heart?

A

-increases the concentration of Ca+2 in muscle fibers, thereby increasing the strength of contraction

183
Q

Arteriovenous fistula

A
  • overloads heart because of excessive venous return

- venous return curve rotates upwward

184
Q

Beriberi

A
  • thiamin deficiency
  • weakening of heart
  • decreased blood flow to kidney -> fluid retention
  • increased mean filling pressure
  • shift return curve to right
185
Q

What are the heart sounds related to?

A
  • first sound -> AV valves close at ventricular systole

- second sound -> semilunar valves close at end of systole

186
Q

What are some common valvular defects?

A
  • valvular lesions
  • rheumatic valvular lesions
  • heart murmurs
  • aortic stenosis
  • aortic regurgitation
  • mitral regurgitation
  • mitral stenosis
187
Q

What are some congenital defects? What is the difference between right to left and left to right?

A
  • left to right: bloods flow backward and fails to flow through systemic circulation
  • right to left: blood flows from right to left side of heart, bypassing lungs
  • patent ductus arteriosus (left to right shunt)
  • tetralogy of Fallot (right to left shunt)
188
Q

What is circulatory shock?

A

-generalized inadequate blood flow through the body, to the extent that body tissues are damaged, especially because of too little oxygen and other nutrients delivered to the tissue cells

189
Q

What are the two ways to reduce cardiac output?

A
  • cardiac abnormalities that decrease the ability of the heart to pump blood
  • factors that decrease venous return
190
Q

cardiac abnormalities reducing cardiac output?

A
  • myocardial infarction
  • toxic state of the heart
  • severe heart valve dysfunction
  • heart arrhythmia
  • circulatory shock that results in diminished cardiac pumping ability -> cardiogenic shock
191
Q

factors that decrease venous return?

A
  • diminished blood volume
  • decreased vascular tone
  • obstruction of blood flow
192
Q

What is the negative feedback mechanism used to return cardiac output and arterial pressure back to normal following cardiac shock?

A

-sympathetic reflexes
+initiated by baroreceptors and other vascular stretch receptors
+result FROM -> decrease in arterial pressure after hemorrhage, decrease in pressures in the pulmonary arteries and veins in the thorax

193
Q

What are the three important effects of the sympathetic reflex?

A
  • arterioles constrict
  • veins and venous reservoirs constrict
  • heart activity increases markedly (160-180bpm)

**autoregulation in cerebral and cardiac vessels maintains more or less normal pressure as long as the arterial pressure does not fall below 70mm Hg

194
Q

What are the factors that causes someone to recover from shock?

A
  • baroreceptor reflexes -> elicit powerful sympathetic stimulation
  • CNS ischemic response -> elicits more sympathetic stimulation until arterial pressure falls below 50mm Hg
  • reverse stress-relaxation of the circulatory system -> causes blood vessels to contract around diminished blood volume so that the blood volume that is available more adequately fills the circulation
  • increased secretion of renin (angiotensin II) -> constricts the peripheral arteries and causes decreased outputs of water and salt
  • increased secretion of vasopression -> greatly increases water retention
  • increased secretion of epi and NE -> increases HR
195
Q

What mechanisms are used to return blood volume back to normal?

A
  • absorption of large quantities of fluid from the interstitial tract
  • absorption of fluids into the capillaries from the interstitial spaces of the body
  • conservation of water and salt by the kidneys
  • increased thirst and appetite for salt
196
Q

What is non-progressive shock?

A
  • sympathetic reflexes and other factors compensate enough to prevent further deterioration of the circulation
  • negative feedback
197
Q

What is progressive shock?

A
  • positive feedback
  • when arterial pressure falls low enough, coronary blood flow decreases below that required for adequate nutrition of the myocardium. Weakens cardiac output and weakens heart muscle more
  • possibly hemorrhagic in origin
198
Q

What are the lethal features of shock?

A

-vasomotor failure
-blockage of small vessels (sludged blood)
-increased vascular permeability
-release of toxins by necrotic tissue
-cardiac depression caused by endotoxin
-generalized cellular deterioration
+decreased sodium and potassium transport
+depressed mitochondrial activity
+breakdown of lysosomes
+depression of cellular metabolism of nutrients

199
Q

What is neurogenic shock?

A
  • shock that occurs without any loss of blood
  • vascular capacity increases so much that even the normal amount of blood becomes incapable of filling the circulatory system adequately
  • one of the major causes of the above is sudden loss of vasomotor tone, resulting in massive dilation of the veins
200
Q

What are some causes of neurogenic shock?

A
  • deep general anesthesia -> depresses vasomotor center to cause vasomotor paralysis
  • spinal anesthesia -> blocks sympathetic nervous outflow
  • brain damage -> causes vasomotor paralysis
201
Q

Difference between osmolarity and osmolality?

A

osmolarity = mOsm/L -> conc of particles per liter of solution

osmolality = mOsm/kg -> conc of particles per kg solvent (water in biological system very similar)

202
Q

What is the effective osmole?

A

-a solute that does not easily cross a membrane. It is an effective osmole because it creates an osmotic force for water.

203
Q

Discuss the intake and output of water.

A

Intake:

  • ingest -> 2100mL/day
  • metabolism -> 200mL/day

Loss:

  • insensible evaporation -> 350mL/day through skin, 350mL/day from lungs
  • sweat -> 100mL/day (5000mL/day with exercise)
  • feces -> 100mL/day
  • urine -> 1400mL/day (500mL/day during exercise)
204
Q

Body fluid compartments and amount of fluid per compartment.

A 
extracellular:
-interstitial (11L)
-plasma (3L)
-transcellular
intracellular
-28L (40%)
205
Q

What is a basal metabolic profile?

A

The concentrations of vital solutes in the body such as;

  • Na
  • K
  • Cl
  • HCO3
  • BUN
  • Cr
  • glucose
206
Q

What is the osmolar gap? What can elevate this?

A
  • helps narrow the differential diagnosis
  • difference between the measured osmolality and the estimated osmolality

Elevated by:

  • ethanol
  • methanol
  • ethylene glycol
  • acetone
  • mannitol
207
Q

What is the indicator-dilution principle?

A

-applies to measurement of fluid volumes in body fluid compartments
-requirements:
+disperses evenly throughout compartment
+disperses only in compartment being measured
+not metabolized or excreted
+not toxic

volume B = indicator volume * indicator conc/ final conc of indicator

208
Q

How do you calculate osmotic pressure of a solution?

A 
-0.9% solution of NaCl
   \+9/58.5 (molecular weight) = 0.308osm/L
   \+osmolarity= 308mOsm/L
-potential osmotic pressure
   \+308mOsm/L * 19.3mm Hg/mOsm/L
   \+ =5944mm Hg

*about 19.3mm Hg osmotic pressure is exerted across the cell membrane

209
Q

Isotonic vs hypotonic vs hypertonic

A
  • isotonic: solutes having osmolarity 228mOsm/L is isotonic, water cannot enter or leave cell
  • hypertonic: solutes have osmolarity greater than 282mOsm/L, water diffuses out of cell
  • hypotonic: osmolarity less than 282mOsm/L, water diffuses into cell
210
Q

How is the brain affected during hyponatremia?

A

acute: acute loss of plasma sodium or excess will cause it to swell
chronic: chronic loss of plasma sodium or excess water allows tissues to transport sodium, chloride, potassium, and other solutes into extracellular spaces. Tissue swelling is less.

211
Q

Relationship between interstitial fluid hydrostatic pressure and interstitial fluid volumes.

A
  • when IF pressure is below 0, little fluid accumulates in tissues. Safety factor against edema is 3mm Hg (pitting edema)
  • when IF pressure rises above 0, free fluid as opposed to gel fluid rapidly begins to accumulate in tissues

Physiology I- Erin (3 decks)

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