Random Questions Flashcards
1
Q
What are the advantages of PEEP?
A
1) Increase driving pressure of oxygen 2) Improves PaO2 without increasing FiO2 3) Allows use of lower FiO2 to achieve same PaO2–> decreasing risk of oxygen toxicity (good for COPD patients) 4) Decreases intrapulmonary shunt by opening collapsed alveoli and increases FRC 5) Decreases surface tension to prevent alveolar collapse at end-expiration
2
Q
What are the disadvantages of PEEP?
A
1) Decreases venous return 2) Increases right ventricular afterload 3) Decreases left ventricular distensibility 4) Decreases cardiac output 5) Barotrauma 6) Increased ICP
3
Q
What type of injury can result from the use of PEEP?
A
Barotrauma from overdistention of alveoli
4
Q
What are the main two reasons for possible water and salt retention related to a patient on mechanical ventilation?
A
aka: arginine vasopressin (AVP) may result from: 1) increased secretion of vasopressin (ADH) 2) decreased levels of atrial natriuretic compound *atrial natriuretic peptide–> inhibits AVP secretion–> in part by inhibiting Angiotensin II-induced stimulation of AVP secretion
5
Q
What is the definition of compliance?
A
measure of distensibility–> expressed as the change in volume for a given change in pressure **involves interrelationship among pressure, volume, and resistance to airflow
6
Q
The peripheral actions of opioids is due to their activation of opioid receptors located where?
A
primary afferent neurons
7
Q
Opioid receptors are normally activated by three endogenous peptide opioid receptor ligands. What are they?
A
1) enkephalins 2) endorphins 3) dynorphins
8
Q
What is the principle effect of opioid receptor activation? How does this occur?
A
a decrease in neurotransmission *occurs largely by presynaptic inhibition of neurotransmitter (aCH, dopamine, norEPI, and substance P) release, although postsynaptic inhibition of evoked activity may also occur
9
Q
The activation of an opioid receptor by an opioid agonist results in one or combination of what two intracellular biochemical events?
A
-EITHER- 1) increased K+ conduction (hyperpolarization) -OR- 2) calcium channel inactivation -OR BOTH- *produces immediate decrease in neurotransmitter release
10
Q
Opioid receptors exist on peripheral ends of the primary afferent neurons… and their activation may either directly _______ neurotransmission or ________ the release of excitatory neurotransmitters, such as substance P.
A
decrease neurotransmission or inhibit release of excitatory neurotransmitters
11
Q
What are the 3 primary opioid receptor classifications?
A
mu, delta, kappa
12
Q
All 3 opioid receptor classes couple to G proteins and have one or combination of what 3 actions?
A
subsequently inhibit adenylate cyclase, decrease the conductance of voltage gated calcium channels, or open inward flowing K+ channels *any of these ultimately results in decreased neuronal activity
13
Q
What two receptors does fentanyl primarily act on?
A
mu (analgesia, respiratory depression, and bradycardia) and kappa (analgesia and sedation)
14
Q
Is fentanyl lipophilic or lipophobic?
A
lipophilic–> highly lipid soluble–> which facilitates transport across the blood brain barrier and its rapid redistribution to non-active tissues like lungs, muscle, and fat–> ultimately means it hangs around in the tissues longer
15
Q
Atrial depolarization is represented by what electrical event on the ECG?
A
P-wave
16
Q
Ventricular depolarization is represented by what electrical event on the ECG?
A
QRS complex
17
Q
Ventricular systole is represented by what electrical event on the ECG?
A
QT interval
18
Q
Ventricular repolarization is represented by what electrical waveform on the ECG?
A
T wave
19
Q
What is a U wave when it appears on the ECG indicative of?
A
-not always present -precise activity unknown; Can be a reflection of hypokalemia
20
Q
What does the term biphasic mean when referring to the SA node and AV node?
A
action potentials in the SA and AV node are biphasic–> meaning they have both a depolarization and repolarization phase and no plateau phase
21
Q
What is the conduction pathway through the heart?
A
SA node (normal pacer)–> Internodal tracts (including AV node and Bachmann’s bundle to left atrium)–> Bundle of His–> Bundle branches–> Purkinje fibers–> Ventricular muscle
22
Q
What is the resting potential of the cardiac ventricular cell?
A
The resting potential of cardiac ventricular cell is -90mV
23
Q
Name the events in the following phase of the ventricular cell action potential: “0”
A
0= rapid depolarization (Na+ diffuses into cell)
24
Q
Name the events in the following phase of the ventricular cell action potential: “1”
A
1= brief repolarization (Cl- diffuses into cell and/or K+ diffuses out)
25
Name the events in the following phase of the ventricular cell action potential: "2"
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2= plateau (Ca++ diffuses into cell)
26
Name the events in the following phase of the ventricular cell action potential: "3"
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3= reploarization (K+ diffuses out of cell)
27
Name the events in the following phase of the ventricular cell action potential: "4"
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4= diastole (Na+-K+ pump operates to restore intracellular Na+ and K+ to appropriate levels)
28
What is the resting potential of the SA node action potential?
-70mV
29
What is the resting potential of the ventricular action potential?
-90mV
30
Name the events in the following phase of the SA node action potential: "0"
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0= slow depolarization (Ca++ and Na+ diffuse into cell)
31
Name the events in the following phase of the SA node action potential: "3"
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3= repolarization (K+ diffuses out of cell)
32
Name the events in the following phase of the SA node action potential: "4"
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4= diastole (spontaneous depolarization to threshold-- diffusion of K+ out of cell decreases progressively and diffusion of Na+ into cell increase progressively; during the last one-third of phase 4, Ca+ ions begin diffuse into the cell)
33
Is there any difference in the action potential of the AV node in comparison to the SA node?
action potential of the AV node has a slower phase 4 depolarization but is otherwise similar to that of the SA node
34
In the SA node action potential, when phase 4 depolarization is slowed (by acetylcholine, for example), what happens to heart rate?
If phase for depolarization is slowed--\> takes longer to reach threshold--\> longer time between action potentials--\> results in a decrease in heart rate \*\*This is what happens during parasympathetic nervous system stimulation by AcH. \*\*So, changing the rate of phase 4 depolarization leads to a change in HR
35
On what phase of the nodal action potential does digitalis work to slow HR?
Phase 4. Digitalis slows phase 4 depolarization of cells in the SA node and AV node.
36
On what phase of the nodal action potential do calcium channel blockers work to slow HR?
Phase 4.... CCB (verapamil, diltiazem, and nifedipine) slow HR by slowing phase 4 depolarization of cells in the SA node and AV node
37
On what phase of the action potential does lidocaine or phenytoin work to control ventricular dysrhythmias?
They suppress spontaneous phase 4 depolarization in ventricular cells (as may occur in ischemic ventricle--\> responsible for PVCs)
38
On what phase of the cardiac ventricular action potential do CCB's work?
CCB's work on phase 2 of the cardiac ventricular action potential; this action is not clinically important, but need to know for EXAM
39
In the cardiac ventricular cell, what is responsible for establishing the resting membrane potential?
potassium
40
What is the name of the "state" for when the gated sodium channel is in an inactivated state in the cardiac cell?
absolute refractory period
41
What is responsible for the plateau phase (phase 2) of the ventricular cell?
calcium entry
42
How is the duration of the phase 2 plateau of the ventricular cell affected by hypocalcemia and hypercalcemia?
calcium ions control the opening of gated K+ channels--\> so....: 1)hypocalcemia--\> duration of the plateau is prolonged 2)hypercalcemia--\> duration of the plateau is shortened
43
What is the length of a normal PR interval?
0.12-0.2 seconds
44
What is the width of a normal QRS interval?
0.12 or \<
45
What is the length of a normal QT interval?
measured from beginning QRS to end of T wave
46
What is a quick method for calculating HR from an EKG based on the R-R interval?
divide 1500 by the number of mm between two consecutive R waves
47
On an EKG, each mm corresponds to ______ seconds.
0.04 seconds
48
What is the normal direction of depolarization of the ventricles?
2 phases: first, depolarization proceeds from the left wall of the septum to the right wall.... second, the ventricles depolarize but the overall spread of depolarization is to the left because the left ventricle is normally electrically predominant
49
How can you diagnose a right bundle branch block?
To make the initial diagnosis, look at leads V1 and V6 in particular. V1 will show an rSR complex (rabbit ears) with a broad R wave. Lead V6 will show a qRS-type complex (deep S waves) with a broad S wave
50
What is electrically occurring to the ventricles during a left bundle branch block?
The septum depolarizes from the right to left (opposite of normal)..... time for left ventricular depolarization will be prolonged, so there will be an abnormally wide QRS complex.... V6 will show a wide, entirely positive R wave with a notch
51
What is the hallmark EKG presentation for first degree heart block?
PR interval is \>0.20 seconds and is constant from beat to beat
52
What is the hallmark presentation on the EKG for second degree AV block Mobitz-Type I (Wenckebach)?
Progressive increase in the PR interval from beat to beat until finally the QRS complex, and a beat, is dropped---\> also associated with a progressive shortening of the R-R interval
53
What is the hallmark presentation on the EKG for a patient in second degree AV block-Mobitz Type II?
rarer and more serious \*sudden appearance of nonconducted P wave. P waves are normal, but some are NOT followed by QRS complexes... PR and RR intervals are constant
54
What is the hallmark presentation on the EKG for third degree heart block (complete HB)?
independent (dissociated) atrial (P) and ventricular (QRS) activity.... P waves have no fixed relationship to the QRS complexes
55
What is the hallmark presentation of sinus arrythmia on the EKG?
\*During inspiration there is an increase in HR because intrathoracic pressure falls--\> consequently, the IVC widens and venous blood pressure falls--\> venous return to the right atrium increases-\> the right atrium stretches and reflexively the HR increases--\> this is the Bainbridge reflex
56
Review Picture on Heart Blocks
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57
Review Picture of PACs
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58
Review Picture of PACs
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59
Peaked or tented T waves on the EKG can reflect \_\_\_\_\_\_\_.
hyperkalemia
60
What changes can be seen on the EKG with hypokalemia?
a decrease in the amplitude of the T wave can result in appearance of a U wave
61
How does hypocalcemia affect the EKG appearance?
Think about what calcium does---\> slower influx of Ca+ prolongs repolarization... so the QT interval will probably be PROLONGED.... the ventricular action potential is prolonged as well d\t the extended phase 2
62
What are the common characteristics of a premature ventricular contraction (PVC)? What is the best treatment?
1) Wide and bizarre
2) QRS complex width \>0.12
3) No P wave
\*1st step--\> correct any underlying abnormalities like hypokalemia or low arterial oxygen tension
\*Lidocaine is then the treatment of choice--\> initial bolus dose of 1.5mg/kg IV; recurrent PVCs can be treated with lidocaine infusion of 1 to 4 mg/min
\*additional treatment: esmolol, propanolol, bretylium, procainamide, quinidine, verapamil, disopyramide, atropine, or overdrive pacing
63
Why should digoxin & verapamil be avoided in a patient with Wolff-Parkinson-White Syndrome?
Avoid in presence of WPW, b\c it increases conduction through the accessory bypass tract (bundle of Kent) and decreases AV node conduction--\> consequently, v-fib can occur; Verapamil should also be avoided since it also increases conduction through the abnormal pathway
\*In WPW, the PR interval is short (\<.12), p wave is normal, rhythm is regular, and HR \<100
64
Evidence of an evolving myocardial infarction is seen in leads II, III, and AVF. What region of the myocardium is involved, and what coronary artery supplies this region?
posterior and inferior walls of the heart may be involved--\> this region is supplied by the right coronary artery
65
What is the best overall lead for myocardial infarction?
V5
66
Evidence of an evolving myocardial infarction is seen in leads V2-V5. What region of the myocardium is involved, and what coronary artery supplies this region?
Septum and anterior wall may be involved--\> left anterior descending (LAD) supplies this area
67
Evidence of an evolving myocardial infarction is seen in leads I, aVL, V4-V6. What region of the myocardium is involved, and what coronary artery supplies this region?
lateral wall may be involved--\> left circumflex supplies this area
68
Review how to measure ST elevation.
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69
Review which leads will have ST elevation in presence of an MI.
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70
Name the leads and coronary artery supply for the following location: Posterior, inferior walls
II, III, aVF--\> RCA
71
Name the leads and coronary artery supply for the following location: Septum, anterior wall
V2-V5--\> LAD
72
Name the leads and coronary artery supply for the following location: Lateral Wall
I, aVL, V4-V6--\> left circumflex
73
What is the formula for stroke volume (SV)?
SV= EDV-ESV
74
What is the formula for ejection fraction (EF)?
(ESV-EDV)/EDV or SV/EDV
75
Which of the following primarily involves pressure? preload or afterload
afterload is "pressure"
76
Which of the following primarily involves volume? preload or afterload
preload involves "volume"
\*preload= EDV, filling of the heart, Starlings Law
77
What two factors are the determinants of mean arterial blood pressure (MAP)?
1) Cardiac Output
2) Systemic Vascular Resistance
78
What two factors are determinants of cardiac output (CO)?
1) heart rate
2) stroke volume
CO= HR x SV
79
Stroke volume is determined by the interplay of three factors. What are they?
1. preload
2. afterload
3. contractility
80
What two factors are the primary determinants of preload?
1. intravascular volume
2. venous tone
\*when the veins constrict, blood is diverted to the heart, and vice versa
81
What is the major determinant of intravascular volume?
the amount of sodium in the body
82
What hormone is MOST important for the controlling of vascular volume?
aldosterone
83
Name and describe the law that relates to preload.
Preload is determined by the VOLUME of blood in left ventricular chamber at end-diastole--\> the GREATER the ventricular filling, the GREATER the PRELOAD--\> when preload INCREASES, stroke volume INCREASES--\> this is the FRANK-STARLING LAW of the heart
84
How does afterload relate to stroke volume?
Inverse relationship--\> As afterload INCREASES, stroke volume DECREASES
\*afterload is the tension (force) in the wall of the heart at the time the aortic valve opens--\> determined by SVR= PRESSURE
85
\_\_\_\_\_\_\_\_ is determined by the chemical environment of the cardiac cell.
contractility--\> contractile functions can be altered by ions (calcium and magnesium), oxygen, acids, drugs, and hormones
## Footnote
\*when contractility increases, the ventricle empties MORE completely and SV INCREASES..... vice versa
86
What are the two primary types of myocardial hypertrophy?
Concentric and Eccentric
87
What law describes ventricular hypertrophy in response to pressure or volume overload?
Law of LaPlace; T= P(r)
88
What is the primary difference between concentric and eccentric hypertrophy?
compared to the normal heart, the size of the left ventricular chamber is NOT changed in concentric but IS changed in eccentric
89
What happens to the left ventricle in a patient with concentric hypertrophy?
There is wall thickening, but normal size of the left ventricular chamber.... its a PRESSURE problem
90
What happens to the left ventricle in a patient with eccentric hypertrophy?
ventricular enlargement..... its a VOLUME problem
91
What are the primary 3 ways that concentric hypertrophy develops?
"develops in response to a PRESSURE overload":
1. chronic untreated HTN
2. chronic aortic stenosis
3. coarctation of the aorta--\> is a congenital condition whereby the aorta narrows in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.
\*IHSS does not apply to this situation
92
What are 3 primary causes of a patient developing eccentric hypertrophy?
"develops in response to a VOLUME overload":
1. chronic aortic regurgitation
2. chronic mitral regurgitation
3. morbid obesity (volume overload state)
93
On the following picture, what is occuring during the segment A:B?
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Diastolic filling.... you can see that volume is increasing and there is a slight rise in pressure
94
On the following picture, what happens at the point "B"?
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The mitral valve closes
95
On the following picture, what is occuring during the segment B:C?
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isovolumetric contraction; the mitral valve is closed so filling has STOPPED and pressure begins to RISE; the EDV is also achieved at point "B"
96
On the following picture, what happens at point "C"?
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Aortic valve opens--\> point "C" is also showing SVR or "afterload"
97
On the following picture, what is occuring during the segment C:D?
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This is the ejection phase of the cycle.... the peak SBP is located at the top of the "hump"
98
On the following picture, what happens at point "D"?
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Aortic valve closes--\> this is also the point signifying ESV
99
On the following picture, what is occuring during the segment D:A?
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Isovolumetric relaxation or "diastole" begins
100
On the following picture, what happens at point "A"?
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Mitral valve opens to begin filling; "diastole"
101
If the LV pressure volume loop is taller or shorter, does this affect preload or afterload?
afterload--\> pressure is changing, which affects AFTERLOAD
102
If the LV pressure volume loop is narrow or wider, does this affect preload or afterload?
preload--\> changes the volume, which affects PRELOAD
103
Where does systole begin and end on the following LV pressure volume loop?
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systole begins at point B and ends at D
104
Where does diastole begin and end on the following LV pressure volume loop?
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diastole begins at D and ends at B
105
How does phenylephrine affect the LV pressure volume loop?
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The afterload is increased because of an increase in the PRESSURE (SVR)
106
If you give fluids to a patient, what normally happens to preload, EDV, ESV, SV and HR?
giving fluids--\> increases preload (filling)--\> increases EDV (filling)--\> no change in ESV--\> increases SV---\> increases BP--\> decreases HR (reflexive)
107
If you give furosemide or Lasix to a patient, what happens to their preload, EDV, ESV, SV, BP, and HR?
give lasix (decreases volume) or nitroglycerin (dilates vasculature)--\> decrease preload (filling)--\> decrease EDV (filling)--\> no change in ESV--\> decrease SV (b\c you decreased preload)--\> decreased BP--\> increase in HR (reflexive)
108
What happens to the LV pressure volume loop when there is an increase (fluids) or decrease (lasix or NTG) in preload?
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## Footnote
If you give fluids that point "B" moves further to the right because the volume at the end of diastole (EDV) is increased... but it still empties out back to the same afterload (ESV) amount at the end of systole.... net increase in SV
109
If you give a patient phenylephrine, what effect does this have on afterload, EDV, ESV, SV, BP, and HR?
give phenylephrine--\> increased afterload (d\t increased SVR-- alpha 1)--\> increased EDV--\> increased ESV--\> decreased SV (increased venous return, increased afterload--\> sandwiches the blood from both ends, decreasing SV)--\> increases BP--\> decreases HR (reflexive)
\*right shift of the loop d\t increased volume.... taller, narrower
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110
If you give a patient nitroprusside (Nipride), what effect does this have on afterload, EDV, ESV, SV, BP, and HR?
give nipride--\> decreases afterload (d\t decrease in SVR)--\> decrease EDV--\> decrease ESV--\> increases SV (d\t decrease in SVR)--\> decrease BP--\> increase in HR (reflexive)
\*you will have decrease in venous return
\*shorter, wider with left shift d\t reduced volume
\*when afterload decreases, the heart empties MORE completely (SV increases)--\> BOTH EDV (preload) and ESV decrease (ventricular chamber shrinks).... when afterload decreases--\> LESS opposing pressure, so less balloon blowing effect on the chambers
111
With an ________ in afterload, the PV loop shifts toward greater pressures and greater volumes (up and to the right).
increase
112
With an ________ in afterload, the PV loop shifts toward smaller pressures and smaller volumes (down and to the left).
decrease
113
What does a semi-closed system refer to?
part of the exhaled gases passes into the atmosphere and part mixes with fresh gases and is rebreathed; chemical absorption of CO2, directional valves, and a reservoir bag are present
114
What does a "closed" system refer to?
complete rebreathing of expired gas; CO2 absorption, reservoir bag, and directional valves are present
115
In a short statement, sum up the difference between an open and closed system?
with an open system the patient gets only what the anesthesia machine provides (mixture delivered by machine); in a closed system the patient rebreaths everything; semi open, semi closed... are all just slight variations allowing partial rebreathing, etc.
116
What is the McMahon system of circuit classification?
uses rebreathing to classify--\> open (no rebreathing), semiclosed (some rebreathing), and closed (total rebreathing)
117
Which of the following offers the most resistance?
Nonrebreathing valve
CO2 canister
Tracheal Tube
Y-piece
Breathing Tube
tracheal tube
118
What are the effects of rebreathing?
reduced loss of heat and water from the patient, reduced inspired oxygen, less fluctuation in inspired anesthetic agent concentration
119
What are factors that can cause a discrepancy between the volume of gas discharged from a ventilator or reservoir bag and that inspired by the patient?
fresh gas flow, compression of gases in the circuit, leaks, distention of breathing system components
120
What are 3 uses of the reservoir bag?
allows use of lower gas flows, provides a means for delivering positive pressure, can serve as a monitor of spontaneous respiration
121
What are common predictors of difficult mask ventilation?
male gender, a beard, lack of teeth, age over 55 yrs, macroglossia, high body mass index, history of snoring, increased MP, and low TM distance; difficult mask is reported in approximately 5-6% of anesthetics
