Concepts/Hemodynamics Flashcards
1
Q
Cardiac output definition
A
amount of blood ejected by the LV in 1 minute.
2
Q
CO may be determined by what test
A
cardiac catheterization
3
Q
CO formula
A
SV X HR
4
Q
Normal CO =
A
4-8 L/min
5
Q
3 factors affecting cardiac output
A
Changes in HR
Changes in contractility
Changes in venous return
6
Q
How does excessive High HR affects cardiac output?
A
excessively high HR, ↓diastolic filling time thus ↓ CO
7
Q
Changes in contractility affect CO how?
A
↑ Sympathetic activity causes ↑ myocardial contractility (positive inotropy) and thus more blood is ejected (↑ SV); this ↑ CO
8
Q
What change in preload affect CO?
A
↑ preload, ↑ force of contraction thus ↑ CO
9
Q
Changes in resistance increase or decrease will affect
A
SV and CO
10
Q
High afterload effect on SV and CO
A
= ↓ SV and ↓ CO
11
Q
Changes in venous return
A
↓ blood volume, ↓ venous return, ↓ preload = ↓ SV and ↓ CO
12
Q
Venous constriction effect on venous return, SV, and CO
A
= ↑ venous return to the heart, ↑ preload,
↑ SV, ↑CO
13
Q
Cardiac index is the
A
CO corrected for differences in body size.
14
Q
CI is based on
A
It is based on body surface area (BSA)
15
Q
CI formula is
A
CI = CO/BSA
16
Q
Normal CI =
A
2.5 - 4L/min
17
Q
2 things that increase CI
A
Exercise
Mild tachydysrhythmias
18
Q
2 things that my decrease CI
A
Decrease myocardiac contractility, MI, CHF, cardiomyopathy and electrolyte imbalance
19
Q
Increase afterload ______CI
A
decrease
20
Q
Things that can increase afterload
A
Valvular stenosis and pulmonary HTN
21
Q
Changes in preload that can decrease CI
A
Hypovolemia
22
Q
How does tachy and irregular rhythm decrease CI
A
↓ diastolic filling time and causes loss of atrial kick.
23
Q
What is Stroke Volume (SV)?
A
SV is the amount of blood ejected by the ventricle with each contraction; the difference between end-diastolic volume and end-systolic volume
24
Q
SV formula
A
EDV-ESV
25
What is ejection fraction?
The percent of how much blood is pushed out of the left ventricle during contraction verses how much was there prior to contraction
26
Normal EF is
greater than 50 % but usually 60-75%
27
Preload is the___? What is it determined by ?
stretch on the myofibrils at the end of diastole; determined by the pressure in the ventricle at the end of diastole.
28
The pressure or volume in the ventricles at the end of diastole.
Preload
29
↑ preload is accomplished by
↑ volume return to the ventricles
30
Evaluation of preload: What evaluated RV preload?
RV preload = CVP or RAP (Right Atrial Pressure)
| Note as preload ↑, myocardial oxygen demand/consumption ↑
31
What evaluates LV preload?
o LV preload = PAOP or LAP (Left Atrial Pressure)
32
Mitral valve stenosis on preload
Increase
33
Mitral insufficiency on preload
Increase
34
Aortic insufficiency on preload
Increase
35
Increase blood volume on preload
Increase
36
Decrease blood volume on preload
Decrease
37
Vasodilators on preload
Decrease
38
Vasoconstrictors on preload
Increase
39
Afterload is the pressure
against which the ventricle must pump to open the
| semilunar valve.
40
Vascular resistance:
o RV afterload =
o LV afterload =
oPVR (Pulmonary Vascular Resistance)
oSVR (Systemic Vascular Resistance)
o Ventricular diameter
o Mass and viscosity of blood
41
Mass and viscosity of blood affect
Vascular resistance
42
As afterload increase, what happens to myocardial oxygen demand/consumption
Increase
43
Aortic valvular stenosis effect on afterload
Increase
44
Aortic valvular stenosis effect on afterload
Peripheral arterial vasonstriction
45
Hypertension effect on afterload
Increase
46
How does polycythemia affect afterload?
Increase
47
Drug that ↓ afterload
Hydralazine
48
Drugs that ↑ afterload:
LED
Levophed
Epinephrine
Dopamine
49
What is the intrinsic rate of a transplanted heart? i.e. non-innervated = no vagus nerve innervation.
120-130 BPM
50
What does Frank Starling’s Law mean?
Starling‟s Law states that the greater the stretch of the cardiac muscle, the more forceful the heart‟s contraction and beat.
51
Frank Starling’s Law limitation, When the muscle is overstretched, the force of contraction may
decrease below normal levels, causing circulatory failure.a rubber band breaking when stretched too far, rendering it useless.
52
Nicotinic receptors are located on
Located on the motor endplate
53
o All neuromuscular blocking agents work here.
Nicotinic receptors.
54
Pulsus paradoxus what is it? How do you treat it? What is in an indication of?
Pulsus paradoxus is an exaggeration of normal physiologic response to inspiration.
55
Pulsus paradoxus normal BP vs BP with inspiration
The normal ↓ BP during inspiration 10 mm Hg or less; therefore a BP ↓ > 10 mm HG during inspiration is pulsus paradoxus.
56
What are three things that PULSUS PARADOXUS INDICATES? Cardiac wise
Pericardial effusion
Constrictive pericarditis
Cardiac tamponade
Advance cardiogenic shock
57
What are three things that PULSUS PARADOXUS INDICATES? other than cardiac
Severe lug disease
advanced heart shock
hemorrhagic shock
58
Main treatment of cardiac tamponade
The main cause is cardiac tamponade and the treatment would be pericardiocentesis.
59
There is a patient having a laminectomy (bloody surgery). The orthopedic physician wants the patient to be hypotensive in order to decrease blood loss. An
ABG is drawn after the case has been going on for 4 hours. The patient is in metabolic acidosis. Why? and what solution (2 possible) ? if the physician ignore and wants pt hypotensive?
The increase blood loss leads to ↓ oxygen carrying capacity
Patient is hypotensive, ↓ peripheral perfusion
This ↓ in O2 capacity and ↓ perfusion causes the body to stop aerobic metabolism and switch to anaerobic metabolism
The byproduct of anaerobic metabolism is LACTIC ACID>.
Return the patient to a normotensive state by giving IVF and blood in order to correct the acidosis.
2. If # 1 does not work, then give NaHCO3
- You must stop the case, because if the patient stays acidotic and hypotensive they will expire.
60
Parasympathetic Nervous System
| Cholinergic: dominant when?
Calm situations
61
Sympathetic Nervous System
| Cholinergic: dominant when?
Crisis situations
62
Promotes activities that restore the body's energy and resources
Cholinergic
63
Promotes activities that prepare the body
| for crisis situations
Sympathetic nervous system
64
Eyes with parasympathetic
Constrict
65
Eyes with Sympathetic
Dilate
66
Parasympathetic on heart
↓ Rate, ↓ contractility
67
Sympathetic on Heart
Heart: ↑ Rate, ↑ contractility
68
Parasympathetic on lungs
bronchoconstriction
69
Sympathetic on lungs
Bronchodilation
70
ParaSympathetic on liver
Glycogenesis
71
Sympathetic on Liver
Glycogenolysis, Lipolysis
72
Parasympathetic on GI
↑ secretion ↑Salivary flow, ↑ Motility,
73
Sympathetic on GI
↓Salivary flow, ↓ Motility, ↓secretion
74
Bladder and parasympathetic
Bladder contracted
75
Sphincter and parasympathetic
Sphincter open
76
Bladder and sympathetic
Bladder relaxed
77
Sphincter and sympathetic
Sphincter closed.
78
Parasympathetic on adrenal gland
No effect
79
Sympathetic on adrenal gland
Secretes epinephrine and norepinephrine
80
First Degree A-V Block definition
o A delay in passage of impulse from the atria to the ventricles.
81
First Degree A-V Block Treatment is
usually unnecessary when it is asymptomatic
82
Second Degree A-V Block definition
Some impulses are conducted and others are not.
83
Second degree AV block Divided into 2 categories:
Type I Wenckebach
| Type II Mobitz
84
Type I Wenckebach usually occurs at? due to ?
Usually occurs at the level of the AV node and is often due to increased parasympathetic tone or to drug effect (digitalis, propranolol, verapamil). It is
85
Type I Wenckeback characteristics
characterized by a progressive prolongation of the PR interval until an impulse is completely blocked.
86
Treatment of 2nd degree AVB type I ? What is priority?
o Treatment is rarely needed unless severe S/S are present. Priority given to identifying cause.
87
Type II Mobitz 2nd Deg AVB.This form of AV block occurs
below the level of the AV node either at the
| bundle of HIS or bundle branches.
88
The hallmark of Type II Mobitz 2nd Deg AVB. block is that the
PR interval does not lengthen before a dropped beat
89
Type II Mobitz 2nd Deg AVB usually associated with
It is usually associated with an organic lesion in the conductive pathway and thus associated with a poorer prognosis and a complete heart block may develop.
90
Treatment (Bradycardia algorithm) of type II Mobitz 2nd deg AVB
Atropine 1 mg rapid IVP: for symptomatic bradycardia
Transcutaneous / Transvenous pacemaker
Catecholamine infusions: Dopamine, Epi, Levophed
Permanent pacemaker.
91
Third Degree A-V Block indicates
Complete absence of conduction between the atria and the ventricles.
92
Treatment of Third Degree A-V Block
Atropine 1 mg rapid IVP: for symptomatic bradycardia
Transcutaneous / Transvenous pacemaker
Catecholamine infusions: Dopamine, Epi, Levophed
Permanent pacemaker
93
Third degree AV block at the AV node may be caused by
increased parasympathetic tone associated with inferior infarction, toxic drug effects (digitalis, propranolol) or damage to the AV node
94
o Third degree AV block at the infranodal level is usually associated with
Infranodal conduction disease. May also be due to coronary atherosclerosis, which is usually associated with an extensive anterior MI.
95
Your patient is in congestive heart failure (CHF). What would you do? What are the signs and symptoms, and treatment?
CHF is a state in which there is impaired cardiac function such that the ventricle is unable to maintain a CO sufficient to meet the metabolic needs of the body.
96
Structures that tend to fail in a patient with CHF?
The LV, RV, or both fail.
97
Left side heart failure: Explain what happens to CO, LV pressure and volume and LV issue?
Is the LA able to empty in the LV? What happens to LA pressure? How does that affect the lungs?
Left sided heart failure
↓ CO, ↑ LV pressure and volume. -LV can‟t pump blood returning from the lungs…
o LA unable to empty into LV thus ↑ LA pressures.
o LA pressure reflected back to lungs producing pulmonary congestion.
98
When pulmonary congestion occurs what happens to pulmonary pressure?
1. Pulmonary pressure causes fluid to leak = pulmonary edema.
2. Oxygenation of blood as O2/CO2 exchange is impeded.
99
o Pressure to lungs : Increase pressure in the right side effects.
↑ pressure to the right side of heart.
o Right heart can‟t pump to lungs due to ↑ pressure in the pulmonary vasculature.
o Venous return impeded as right side of heart fails
o As Pressure builds, body organs become congested with venous blood.
100
o Right-sided heart failure may occur first in the case of
RV infarcts.
101
Top causes of Left sided heart failure; be able to say at least first 4
1. Acute LV MI
2. Cardiomyopathy
3. Atherosclerotic heart disease
4. ↑ circulating volume
5. Aortic stenosis/insufficiency
6. Cardiac tamponade
7. Mitral stenosis/ insufficiency
8. Tachy/Bradycardia
102
Top causes of Right sided heart failure: be able to say at least first 4
1. Left-sided heart failure
2. Atherosclerotic heart disease
3. Acute RV MI
4. Tachy/Bradycardia
5. Pulmonary embolism
6. Fluid overload
7. Excess sodium intake
8. Mitral stenosis
9. Atrial or ventricular septal defect
10. Pulmonary outflow stenosis
11. COPD
12. Pulmonary hypertension
13. Cor Pulmonale
103
Cor pulmonale is HF due to
Lung pathology
104
General symptoms /Clinical Manifestations of HF
Chest discomfort, SOB, orthopnea, paroxysmal nocturnal dyspnea, weight gain, ↓ urination, edema
105
Right sided HF signs and symptoms
```
Right Depend E JAH
Dependent edema
JVD
Ascites
Hepatomegaly
```
106
Left sided HF signs and symptom s
```
Orthopnea
Cyanosis
Hypoxia
Dyspnea
More systemic signs
```
107
Cough with Frothy sputum is sign of what kind of HF
LEFT
108
Treatment of HF
Cardiac glycosides and AMRINONE
109
Amrinone mechanism of action
| - cardiac contractility
↑ cardiac contractility without ↑ rate by ↑ cellular levels of cyclic AMP
110
Amrinone and vascular smooth
Relaxes vascular smooth muscle producing peripheral vasodilation (↓ preload and ↓ afterload
111
Amrinone bolus and infusion
Initial bolus 0.75-1.5 mcg/kg over 2-3 min followed by infusion 5-10 mcg/kg/min.
112
Vasodilators action in patient with HF
improve LV function by lowering systemic vascular resistance: ↓ afterload
o Nitroglycerin
o Nitroprusside
113
What is a quick fix for hyperkalemia?
Glucose, insulin and NaHCO3:
114
Action of Glucose insulin and bicardbonate in HYPERKalemia
temporarily drive K+ into cell
115
Why give NaCO3, how does it drive K+ into the cell?
Because the cells are trying to compensate for the acidic environment by exchanging K+ out of the cell and H+ into the cell
116
Ca++ Chloride or Ca++ gluconate IV to stimulate
cardiac contractility: contraindicated in patients on digoxin
117
After giving insulin , glucose and. NaHCo3
Follow up with Kayexalate and sorbitol or HD for permanent removal
118
Calcium is contraindicated in what kind of patients
DIGOXIN
119
What is angina and how do you treat it?
| o Angina-
a state of transient myocardial ischemia without cell death
120
Ischemia- Local and temporary deficiency of blood supplies due to
obstruction of circulation to a part. Ischemia leads to anaerobic metabolism and accumulation of lactic acid, causing chest pain
121
Epinephrine is used to
used to ↑ CO by ↑ HR, resulting in an ↑ in cerebral and coronary blood flow and an ↑ in SVR
122
First-line drug for any pulseless rhythm
Epinephrine
123
Epinephrine dose
1 mg IV push Q 3-5 minutes.
124
Epinephrine CO, PAOP, SVR, MAP, HR, CVP and PVR
↑ CO, ↑PAOP, ↑SVR, ↑MAP, ↑HR, ↑CVP, ↑PVR
125
Epinephrine dose infusion
1 - 4 mcg/min
126
A natural catecholamine that is the immediate precursor of norepinephrine
Dopamine
127
When is dopamine used?
It is used to ↑ low BP refractory to fluid therapy, to treat heart failure, increase renal perfusion, and correct hemodynamic imbalance in shock syndrome.
128
Dopamine Onset and duration
5 minutes, duration 10 minutes.
129
Low dose dopamine
Low dose (renal perfusion) + 1-3 mcg/kg/min
130
Dopamine Medium dose
(↑ contractility) = 3-10 mcg/kg/min. (Vasoconstriction) > 10 mcg/kg/min.
131
Dopamine side effects at high doses
May induce myocardial ischemia. Nausea and vomiting especially at high doses
132
Relative Contraindications to the use of dopamine
o The presence of ↑ vascular resistance, pulmonary congestion, or ↑ preload is a relative contraindication to the use of dopamine
133
Dopamine precautions at high doses
o Renal ischemia at high doses.
| o Tissue sloughing if IV infiltrates
134
High dose of dopamine (works like Levophed)
> 20 mcg/kg/min
135
Dobutamine (Dobutrex)
Synthetic sympathomimetic catecholamine with inotropic, chronotropic and vasodilator effects.
136
What receptors does dobutamine stimulates?
It stimulates β1 and α1 receptors.
137
When to use dobutamine?
Useful in treating heart failure (especially with ↑ SVR and PVR), to increase contractility with no significant increase in heart rate.
138
Dopamine vs dobutamine
It is similar to dopamine but does not cause a significant rise in BP.
139
Dobutamine actions on CO, PAOP, SVR, MAP, HR, CVP and PVR
↑ CO, ↓ PAOP, ↓ SVR, ↑ MAP, ↑ HR (slowly), ↓ CVP, ↓P
140
Dobutamine infusion rate
Infuse at 2-10 mcg/kg/min. May go up to 40 mcg/kg/min. with MD approval.
141
This medication May induce myocardial ischemia.
Dobutamine
142
SE of Dobutamine
HA, nausea, tremor and ↓ K+
143
Atropine is an _____how does it work?
An anticholinergic parasympathetic. (Muscarinic receptors) It ↑ CO and ↑ HR by blocking cardiac vagal stimulation in the heart.
144
Atropine used in
Used in bradycardia and bradydysrhythmias, blocking cardiac vagal reflexes (also to ↓ secretions and broncodilitation)
145
Atropine dose
IV: give 1 mg q 3-5 minutes, not to exceed 3 mg.
| Give rapid IVP as pushing slowly may cause paradoxical bradycardia lasting 2 minutes.
146
Morphine is a
Narcotic analgesis
147
3 main action of morphine
It relieves pulmonary congestion, lowers myocardial O2 consumption, and reduces anxiety.
148
Analgesia of choice in pain associated with MI.
Morphine
149
Morphine on veins and preload
Dilates veins and ↓ preload.
150
SE of Morphine
Side effects include respiratory depression, hypotension, ↑ ICP, N/V.
151
Antidote of morphine
Narcan.
152
Nipride (Nitroprusside). What is it and what is the action on CO, LV and BP
A venous and arterial dilator used to ↑ CO by ↓ LV afterload, to ↓ blood pressure in hypertensive crisis, and to ↓ pulmonary hypertension
153
Nitroprusside actions on CO, PAOP, SVR, MAP, HR, CVP and PVR
↑ CO, ↓ PAOP, ↓ SVR, ↓ MAP, ↑ HR, ↓ CVP, ↓ PVR Infuse
154
Nitroprusside dosing
0.5 – 10 mcg/kg/min.
155
How long is nitroprusside solution stable for
24 hours
156
What should you check for nitroprusside? when?
Check thiocyanate level if infusion continues longer than 72 hour or if rate ≥ 4 mcg/kg/min.
157
Signs of Nitroprusside toxicity
Almond breath Antidote: Amyl nitrate inhaled, NA thiosulfate IV.
158
Nitroglycerin (Tridil) What is it and what is it used for?
A venous vasodilator used to ↓ preload and afterload in LV failure. It is also used for myocardial ischemia and as a dilator for coronary vasculature.
159
NTG dosing
There is no optimum fixed dose. Titrate to response. Most patients respond to 50 – 200 mcg/min.
160
NTG precautions.
Precautions: When piggybacking, do so close to the insertion site as tubing can absorb 40% -80% of drug.
161
Nitroglycerin solution stable for ? how about tolerance
Solution stable only 24 hours
| Patients develop tolerance over 1-2 days.
162
Patient has hyponatremia, why?
Hyponatremia is when an excess of water relative to the amount of sodium in the body produces a dilutional effect on sodium concentrations.
163
What is hyponatremia?
Sodium < 136
164
SIADH is a
condition characterized by impaired renal excretion of water, resulting in oliguria, high urine specific gravity, water intoxication and hyponatremia.
165
Other causes of hyponatremia include:
|
Sodium depletion
Diuretics
Diarrhea
Nasogastric suction
Abnormal losses via diaphoresis
Salt-losing renal diseases: interstitial nephritis
Hyperglycemia (glucose induced diuresis)
166
Other causes of hyponatremia include:
|
* Sodium depletion
* Diuretics
* Diarrhea
* Nasogastric suction
* Abnormal losses via diaphoresis
* Salt-losing renal diseases: interstitial nephritis
* Hyperglycemia (glucose induced diuresis)
167
Kidneys when there is excess sodium?
o Kidneys may retain larger amounts of water in excess of sodium
168
Normal ICP
0-15 mmHg
169
CPP (Cerebral perfusion pressure)
CPP = MAP – ICP
170
What does CPP represents?
This represents the pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery
171
CPP normal pressure
o Normal 70-100 mmHg
172
Trace the path of blood through the heart
```
Inferior, Superior (Common) Vena cava
↓
Right Atrium
↓
Tricuspid Valve
↓
Right Ventricle
↓
Pulmonic Valve
↓
Pulmonic Artery
↓
Lungs
↓
Pulmonary Vein
↓
Left Atrium
↓
Mitral (Bicuspid) Valve
↓
Left Ventricle
↓
Aortic (Semilunar) Valve
↓
Aorta
↓
Systemic Circulation
```
173
Describe the relationship between CO2 and a head injury.
A PaCO2 of 30-35 mmHg (moderate hyperventilation) causes vasoconstriction (arterial) and thus decreases cerebral blood volume. Decreasing the cerebral blood volume will decrease the intracranial pressure. CO2 is a potent vasodilator.
174
If you continue to hyperventilate the patient in 12 hours will they still be vasoconstricted?
Yes
175
OxyHemoglobin Dissociation Curve
| This curve describes the relationship between
available oxygen and amount of oxygen carried by hemoglobin.
176
Horizontal axis and vertical axis of the oxyhemoglobin dissociation curve.
The horizontal axis is Pa02, or the amount of oxygen available. The vertical axis is SaO2, or the amount of hemoglobin saturated with oxygen.
177
Once the PaO2 reaches 60 mm Hg the OxyHgb dissociation curve is
almost flat, indicating there is little change in saturation above this point.
o So, PaO2 of 60 or more is usually considered adequate.
178
OxyHgb dissociation curve at less than 60 mmHg
less than 60 mm Hg the curve is very steep, and small changes in the PaO2 greatly reduce the SaO2. The term "affinity" is used to describe oxygen's attraction to hemoglobin binding sites.
179
OxyHgb dissociation curve at less than 60 mmHg
less than 60 mm Hg the curve is very steep, and small changes in the PaO2 greatly reduce the SaO2.
180
The term "affinity" is used to describe
oxygen's attraction to hemoglobin binding sites.
181
Oxyhgb Affinity changes with
* variation in pH,
* temperature,
* CO2 and,
* 2,3,-DPG
* a metabolic by-product which competes with O2 for binding site
182
Traditionally the curve starts with:
* pH at 7.4,
* temperature at 37 Centigrade, and
* PaCO2 at 40.
* Changes from these values are called "shifts".
183
A left shift will on oxyhgb
increase oxygen's affinity for hemoglobin.
| o In a left shift condition (alkalosis, hypothermia, etc.) oxygen will have a higher affinity for hemoglobin.
184
With a left shift, SaO2 will increase at a
given PaO2, but more of it will stay on the hemoglobin and ride back through the lungs without being used. This can result in tissue hypoxia even when there is sufficient oxygen in the blood.
185
A right shift and affinity
decreases oxygen's affinity for hemoglobin.
186
o In a right shift (acidosis, fever, etc.) oxygen has a ____What does it means?
lower affinity for hemoglobin. Blood will release oxygen more readily.This means more O2 will be released to the cells, but it also means less oxygen will be carried from the lungs in the first place.
187
Temperature- Increasing the temperature does what?
denatures the bond between oxygen and hemoglobin, which increases the amount of oxygen and hemoglobin and decreases the concentration of oxyhemoglobin. The dissociation curve shifts to the right.
188
pH- A decrease in pH (increase in acidity) by addition of carbon dioxide or other acids causes a
Bohr Shift.
189
A Bohr shift is characterized by
causing more oxygen to be given up as oxygen pressure increases and it is more pronounced in animals of smaller size due to the increase in sensitivity to acid
190
The ejection fraction is a
measurement of the heart's efficiency and can be used to estimate the function of the left ventricle, which pumps blood to the rest of the body.
191
The left ventricle pumps only a fraction of the blood it contains. The ejection fraction is the
amount of blood pumped divided by the amount of blood the ventricle contains.
192
A normal ejection fraction is more than
55% of the blood volume.
193
If the heart becomes enlarged, even if the amount of blood being pumped by the left ventricle remains the same, the relative
fraction of blood being ejected decreases.
194
A healthy heart with a total blood volume of
100 mL that pumps 60 mL to the aorta has an ejection fraction of 60%.
195
Define PEEP.
Positive end expiratory pressure (PEEP) is a mode of therapy used with mechanical ventilation. At the end of exhalation the patient‟s airway pressure is maintained above atmospheric pressure. The purpose is to prevent alveolar collapse at end expiration.
196
Benefits of PEEP
o Improve functional residual capacity (FRC)
| o Enhance oxygen transport (allows for > PaO2 without requiring ↑ FI
197
What are the complications of PEEP?
Complications
o Impaired venous return, resulting in ↓ C.O.
o ↓ venous return, ↓C.O. ↓O2 delivery even though ↑ PaO2
o Barotrauma- rupture of lung tissue. PEEP levels >15 cm H2O are considered dangerous (tension pneumo).
198
Blood goes from
High pressure (Arteries) to Low pressure (Venous)
199
Pulse ox reads Hgb saturation in the
arteries.
200
Anterior Cerebral Artery supplies what lobes?
o Supplies frontal and Parietal Lobes
| o Supplies leg area of precentral gyrus
201
Middle Cerebral Artery (MCA)
Supplies most of the basal ganglia and parts of internal capsule.
202
Supplies almost all cortical surface of brain.
MCA
203
Internal Carotid Artery
o Supplies portions of basal ganglia
| o Supplies part of internal capsule.
204
o Supplies Circle of Willis
Internal Carotid Artery
205
Supplies anterior portion of the circle of willis
Anterior Communicating Artery
206
o Supplies medial occipital lobes and medial temporal lobes
| o Supplies thalamus
Posterior Cerebral Artery
207
Which branch of the circle of willis Supplies Thalamus
Posterior Cerebral Artery
208
Which branch of the circle of willis Supplies Thalamus
Posterior Cerebral Artery
209
o Supplies medial occipital lobes and medial temporal lobes
Posterior Cerebral Artery
210
Supplies upper surface of Cerebellum and midbrain
Superior Cerabellar Artery
211
Basilar artery
• AICA Anterior Inferior Cerabellar Artery
Undersurface of Cerebellum and pons
•PICA Posterior Inferior Cerabellar Artery
o Undersurface of Cerebellum and Midbrain
212
Olfactory Nerve
o Sensory
| o Smell
213
II. Optic Nerve
o Sensory
| o Vision
214
III. Ocular Motor Nerve
o Motor
•Most EOM movement, raise eyelids
o Parasympathetic:
• Pupilary constriction, Lens shape
215
IV. Trochlear Nerve: Sensory or Motor
Motor
| • Down and inward movement of the eye
216
V. Trigeminal Nerve
o Motor
• Muscles of mastication
o Sensory
• Sensation of face and scalp, cornea, mucous membranes of mouth and nose
217
VI.Abducens Nerve
o Motor
| • Lateral eye movement
218
VII. Facial Nerve
o Motor
Facial muscles, close eye, labial speech
o Sensory
Taste (sweet, salty, sour, bitter) on anterior two-thirds of tongue
o Parasympathetic
Saliva and tear secretion
219
VIII. Acoustic nerve
o Sensory
| Hearing and Equilibrium
220
Glossopharyngeal
o Motor
Pharynx (phonation and swallowing)
o Sensory
Taste on posterior one-third of tongue, pharynx (gag reflex)
221
Parasympathetic of glossopharyngeal
• Parotid gland, carotid reflex
222
Vagus Nerve Motor and Sensory
o Motor
• Pharynx and Larynx (talking and swallowing)
o Sensory
• General sensation from carotid body, carotid sinus, pharynx, viscera
o Parasympathetic
Carotid reflex
223
VI. Spinal Nerve
Motor
| Movement of trapezius and sternomastoid muscle
224
VII. Hypoglossal
o Motor
| Movement of tongue
225
The Patient is vented and has an ABG reading with a PaO2 of 130 on FiO2 50%. Some thing is wrong, PaO2 should be higher than 130.What may be causing the ↓ oxygenation?
o Right mainstem intubation
o Atelectasis
o ↓ CO
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Signs and Symptoms of ↑ ICP.
| What are early interventions that you can perform as a nurse to ↓ ICPs prior to any MD orders?
o ↓ Stimulation
↓ sympathetic stimulation, ↓ HR, ↓ BP = ↓ ICP
Reverse Trendelenburg
Proper neck alignment
A flexed head will increase ICP by constricting venous drainage.
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NeuroTransmitters Excitation is the
response of the subsynaptic membrane to the neurotransmitter substance that lowers the membrane potential to form an excitatory postsynaptic potential. Sodium ions rush into the neuron, whereas potassium ions leave the cell trough the postsynaptic membrane.
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Inhibition acts on a cell so that it is
more difficult for it to fire.
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The membrane potential is raised to form the
inhibitory postsynaptic potential.
230
The inhibitory neurotransmitters
increase permeability to only potassium and chloride ions in the synaptic membrane.
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Acetylcholine
| o Usually excitatory, it is found in the
motor cortex, skeletal muscle, preganglionic autonomic nerves, postganglionic parasympathetic nerves, and postganglionic sympathetic nerves to sweat glands.
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Acetylcholine
| Usually excitatory, it is found in the
motor cortex, skeletal muscle, preganglionic autonomic nerves, postganglionic parasympathetic nerves, and postganglionic sympathetic nerves to sweat glands.
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Muscarinic receptors
Are located in all of the postganglionic parasympathetic endings and the postganglionic sympathetic endings to sweat glands.
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o Chief neurotransmitter of the parasympathetic nervous system
ACH
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Norepinephrine
o Usually excitatory, and found in the postganglionic sympathetic nerves.
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o Chief neurotransmitter of the sympathetic nervous system
NE
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Dopamine
| ______Effectst
o Inhibitory
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o Affects control of behavior and fine movement
Dopamine
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o Adrenergic receptors
Norepinephrine stimulates alpha > beta.
| Epinephrine stimulates alpha and beta equally
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Can be synthesized to NE to EPI
| o Dopaminergic receptors
Dopamine
241
Can be synthesized to NE to EPI
Dopamine; Dopaminergic receptors
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