Random Questions Flashcards
What are the advantages of PEEP?
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
What are the disadvantages of PEEP?
1) Decreases venous return 2) Increases right ventricular afterload 3) Decreases left ventricular distensibility 4) Decreases cardiac output 5) Barotrauma 6) Increased ICP
What type of injury can result from the use of PEEP?
Barotrauma from overdistention of alveoli
What are the main two reasons for possible water and salt retention related to a patient on mechanical ventilation?
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
What is the definition of compliance?
measure of distensibility–> expressed as the change in volume for a given change in pressure **involves interrelationship among pressure, volume, and resistance to airflow
The peripheral actions of opioids is due to their activation of opioid receptors located where?
primary afferent neurons
Opioid receptors are normally activated by three endogenous peptide opioid receptor ligands. What are they?
1) enkephalins 2) endorphins 3) dynorphins
What is the principle effect of opioid receptor activation? How does this occur?
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
The activation of an opioid receptor by an opioid agonist results in one or combination of what two intracellular biochemical events?
-EITHER- 1) increased K+ conduction (hyperpolarization) -OR- 2) calcium channel inactivation -OR BOTH- *produces immediate decrease in neurotransmitter release
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.
decrease neurotransmission or inhibit release of excitatory neurotransmitters
What are the 3 primary opioid receptor classifications?
mu, delta, kappa
All 3 opioid receptor classes couple to G proteins and have one or combination of what 3 actions?
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
What two receptors does fentanyl primarily act on?
mu (analgesia, respiratory depression, and bradycardia) and kappa (analgesia and sedation)
Is fentanyl lipophilic or lipophobic?
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
Atrial depolarization is represented by what electrical event on the ECG?
P-wave
Ventricular depolarization is represented by what electrical event on the ECG?
QRS complex
Ventricular systole is represented by what electrical event on the ECG?
QT interval
Ventricular repolarization is represented by what electrical waveform on the ECG?
T wave
What is a U wave when it appears on the ECG indicative of?
-not always present -precise activity unknown; Can be a reflection of hypokalemia
What does the term biphasic mean when referring to the SA node and AV node?
action potentials in the SA and AV node are biphasic–> meaning they have both a depolarization and repolarization phase and no plateau phase
What is the conduction pathway through the heart?
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
What is the resting potential of the cardiac ventricular cell?
The resting potential of cardiac ventricular cell is -90mV
Name the events in the following phase of the ventricular cell action potential: “0”
0= rapid depolarization (Na+ diffuses into cell)
Name the events in the following phase of the ventricular cell action potential: “1”
1= brief repolarization (Cl- diffuses into cell and/or K+ diffuses out)
Name the events in the following phase of the ventricular cell action potential: “2”
2= plateau (Ca++ diffuses into cell)
Name the events in the following phase of the ventricular cell action potential: “3”
3= reploarization (K+ diffuses out of cell)
Name the events in the following phase of the ventricular cell action potential: “4”
4= diastole (Na+-K+ pump operates to restore intracellular Na+ and K+ to appropriate levels)
What is the resting potential of the SA node action potential?
-70mV
What is the resting potential of the ventricular action potential?
-90mV
Name the events in the following phase of the SA node action potential: “0”
0= slow depolarization (Ca++ and Na+ diffuse into cell)
Name the events in the following phase of the SA node action potential: “3”
3= repolarization (K+ diffuses out of cell)
Name the events in the following phase of the SA node action potential: “4”
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)
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
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
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.
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
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)
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
In the cardiac ventricular cell, what is responsible for establishing the resting membrane potential?
potassium
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
What is responsible for the plateau phase (phase 2) of the ventricular cell?
calcium entry
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
What is the length of a normal PR interval?
0.12-0.2 seconds
What is the width of a normal QRS interval?
0.12 or <
What is the length of a normal QT interval?
measured from beginning QRS to end of T wave
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
On an EKG, each mm corresponds to ______ seconds.
0.04 seconds
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
Review Picture on Heart Blocks
Review Picture of PACs
Review Picture of PACs
Review how to measure ST elevation.
Review which leads will have ST elevation in presence of an MI.
On the following picture, what is occuring during the segment A:B?
Diastolic filling…. you can see that volume is increasing and there is a slight rise in pressure
On the following picture, what happens at the point “B”?
The mitral valve closes
On the following picture, what is occuring during the segment B:C?
isovolumetric contraction; the mitral valve is closed so filling has STOPPED and pressure begins to RISE; the EDV is also achieved at point “B”
On the following picture, what happens at point “C”?
Aortic valve opens–> point “C” is also showing SVR or “afterload”
On the following picture, what is occuring during the segment C:D?
This is the ejection phase of the cycle…. the peak SBP is located at the top of the “hump”
On the following picture, what happens at point “D”?
Aortic valve closes–> this is also the point signifying ESV
On the following picture, what is occuring during the segment D:A?
Isovolumetric relaxation or “diastole” begins
On the following picture, what happens at point “A”?
Mitral valve opens to begin filling; “diastole”
Where does systole begin and end on the following LV pressure volume loop?
systole begins at point B and ends at D
Where does diastole begin and end on the following LV pressure volume loop?
diastole begins at D and ends at B
How does phenylephrine affect the LV pressure volume loop?
The afterload is increased because of an increase in the PRESSURE (SVR)
What happens to the LV pressure volume loop when there is an increase (fluids) or decrease (lasix or NTG) in preload?
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
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
