Test 3 Flashcards
(171 cards)
1
Q
where do PE usually arise from
A
thrombi in the deep venous system of the lower extremities
2
Q
What veins are responsible for most PEs
A
Ileofemoral
3
Q
Most PEs are multiple goes to what part of the lung
A
lower lobes b/c of gravity
4
Q
risk factors to develop PE
A
immobilization (#1 reason), surgery in last 3 months. stroke, cancer, obesity, history of thrombi, smoking, HTN, BC
5
Q
What are the 2 most common causes of inherited thrombosis?
A
Factor V Leinden mutation, and prothrombin gene
6
Q
common symptoms of PE
A
SOB, pleurtic pain, cough, hemoptysis, sometimes no symptoms
7
Q
common signs of PE
A
tachypnea, crackles, tachy, hear 4th heart sound (la da dub), ABG may have normal pO2, resp alkalosis is common
8
Q
D Dimer test for PE
A
detectable at levels >500 in patients with Pe, not sufficient to diagnose PE, if it comes back negative that proves there is no PE
9
Q
Pulmonary angiogram test for PE
A
rarely used at large centers but remain the definitive diagnostic test
10
Q
What tool is usually used to help diagnose a PE
A
CT Scan
11
Q
Treatment for PE
A
heparin followed by warfarin. usually use LMW heparin, alternative are Eliquis or Zerelto which are factor Xa inhibitors
12
Q
when is a surgical embolectomy used?
A
embolism is trapped in the RA of RV or in patent foramen ovale, or cant take thrombolytic therapy
13
Q
how do you diagnose chronic pulmonary thrombosis
A
chest xray (R. heart failure, pleural disease, large pulmonary arterties), PFT, pulmonary HTN on echo, hypoxemic on ABG, CT scan is better at defining segmental disease**
14
Q
the respiratory center is located where?
A
medulla and pons
15
Q
what are the 3 main components of the respiratory center
A
medullary center (maintains normal resp. pattern), apneustic center, and pneumotaxic center (last 2 work together to maintain volume and rate)
16
Q
how does the respiratory center receive its info?
A
receive input for O2 sensors in the carotid bodies, H+ sensors in the brain stem, mechanoreceptors in the lung, and the cerebral cortex and they all interpret info and send signal to brain
17
Q
what are the oxygen chemoreceptors?
A
carotid bodies and aortic bodies, inc output brain says to breathe faster
18
Q
What are the CO2 chemoreceptors
A
ventral surface of medulla which responds to H+ ions in CHF
19
Q
phrenic nerve does what?
A
helps with diaphragm function, arises from C3-5
20
Q
what do the intercostal nerves do?
A
play a role in breathing and arise from T1-12
21
Q
what are the abdominal muscle nerves for?
A
dont really need except when breathing heavy/traume, arise from T7-L1
22
Q
what do the neuromuscular junction do?
A
releases acetylcholine which causes muscle to contract
23
Q
what is the main muscle used in inspiration?
A
diaphragm (#1), then external intercostals, scalene, sternocleidomastoid
24
Q
what are the muscles used in expiration?
A
internal intercostals, abdominal wall
25
what is the most common form of hypoxemia?
V/Q mismatch
26
clinical features of Neuro Disease
SOB, CO2 retention, reduced capacity for exercise, dec. pH, hypoxemia due to V/Q mismatch,
27
What do you want to watch the progression for in patients with neuomus. Disease
dec VC <-20
28
what is the number 1 cause of why the diaphragm wouldnt work?
nerve trauma
29
What can cause unilateral paralysis
trauma, lesions
30
what happens where their is unilateral paralysis of diaphragm
SOB, absence of BS over the lower chest on affected side, crackles near compressed lung, dec. excursion, elevated hemidiaphragm on xray
31
How do you diagnose unilateral paralysis?
Sniff test with fluoroscopy or ultrasound
32
Bilateral paralysis of diaphragm
dyspnea at rest. usually require MV
33
above C3 on the spine produces what?
complete resp. musc. paralysis
34
what is poliomyelitis?
virus that destorys motorneurons in the anterior horn of the spinal cord (used iron lung ventilation)
35
Guillain Barre Syndrome
preceded by viral type of illness, inflammation of spinal roots and peripheral nerves which causes destruction of myelin sheaths
36
GBS is known to be what type of paralysis?
progressive ascending (feet to head)
37
what can cause GBS
infectious mononucleosis, flu, measles, mumps, hepatitis, salmonella, chlamydia
38
GBS usually affects who?
greater than 45 yo, males, whites almost 90% recover
39
signs of GBS
CSF shows inc protein with normal cell count (inc. lymphocytes), nerves conduction studies are helpful, fever, malaise, numbness, paralysis peaks in 10 days, sensory impairment, cyanosis, dec lung vol and BS, normal xray
40
treatment of GBS
stabilize VS, oxygen, mobilize secretions, prevent DVT, prevent skin breakdown, hyperinflation, MV, Plasmapheresis or IV immunoglobulin
41
Amyotrophic lateral sclerosis (Lou Gerhigs Disease)
progressive subacute neuromusc disease, loss of motor neurons in anterior horn, cause is UK, no treatment
42
Myasthenia gravis
chronic disorder affected the neuromuscular junction, interferes with transmission of acetycholine, caused by anti ACh receptor antibodies, thymus gland is usually abnormal
43
how do you diagnose MG
tensilon test (helps stop breakdown of acetycholine), EMG, and measure circulation anti ACh antibodies
44
ventilatory failure of MG usually happens when
after surgery (thymectomy)
45
Myasthenic crisis is what/
disease that affects the muscles
46
what is a cholinergic crisis
happens when overtreating MG
47
how do you treat MG
mobilize secretions, O2, hyperinflation, steroids, Mestinon, thymectomy, plasmapheresis in acute MG and azathiaprine in chronic MG
48
Botulism
severe paralytic disease caused by botulinal toxin produced by clostridial species, most potent poison to man
49
botulism has what type of paralysis
descending
50
What needs to be tested for Botulism?
serum, stool, gastric contents, or food
51
signs/symptoms of botulism
dry mouth, sore throat, ileus, urine retention, nausea, vomiting, and stomach pain
52
Treatment of Botulism
observe for vent support, gastro purge, antitoxin, guanidine hydochloride
53
quaternary organophosphate poisoning
muscle paralysis, inhibit acetylcholinesterase
54
how do you treat QOP
atropine**
55
Strychnine
common dilutant of street drugs, blocks inhibitory neurons in spinal cord, global musc spasm
56
how do you treat strychnine
phenobarb, valium, paralyze and intubate
57
Tetanus
neurotransmitter blockade is an effect, severity progresses over days
58
how do you treat tetanus
sedation, muscle relaxers, intubate with MV
59
Muscular dystrophy
gradual onset of resp. muscle weakness, duchenne and steinert forms have an impaired control of breathing
60
what is the number one cause of lung cancer?
smoking
61
What are the types of lung cancer
non small cell (squamous, adenocarcinoma, large cell) and small cell
62
symptoms of lung cancer
usually presents too late, cough, SOB, hemoptysis, chest pain, weight loss, no symptoms
63
when lung cancer metastisizes where does it go?
bone (spine most common), liver, brain, adrenal glands
64
staging of non small cell
try to cut out, TNM (t= characteristics of tumor, N=lymph node involvement, M= metastasis)
65
stagging of small cell
rapid growing, ipsilateral hemithorax is limited disease and beyone ipsilateral hemithorax is extenstive disease, treat with chemo/rad
66
what is EBUS test
bronchoscope with US tip on end, used to sample lymph nodes for cancer
67
treatment for stage 1 non small cell
surgical resection
68
treatment for stage 2 non small cell
surgical resection with XRT or chemo
69
treatment for stage 3a non small cell
surgical resections with combo chemo
70
treatment for stage 3b non small cell
chemo, XRT, palliation
71
treatment for stage 4 non small cell
chemo, palliation
72
Treatment for small cell
solitary nodules can be treated with surgery, systemic chemo
73
what is the stronger predictor of post op complications of non small cell surgery
FEV1
74
what type of surgery is most common is non small cell cancer
lobectomy and also take out lymph nodes
75
When is a pneumonectomy used for non small cell
proximal CA or if tumor crosses the fissure
76
When is wedge resection used for non small cell
only if poor lung function ( dec cure), usually dont take out lymph nodes
77
chemo and XRT prior to surgery does not help what stage of non small cell
1 or 2
78
how do you treat limited disease of small cell cancer
concurrent chemo and XRT
79
how do you treat extensive disease of small cell cancer
aggressive combo chemo
80
definition of shock
physiological state characterized by significant systemic reduction in tissue perfusion, resulting in dec tissue oxygen delivery
81
shock results in what?
cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents, inadequate regulation of pH
82
mortality is highest is what type of shock
cardiogenic
83
tissue perfusion is determined by what?
SVR and CO (help distinguish different forms of shock)
84
features of shock
Hypotension, cool/clammy skin, low urine output, change in mental status, metabolic acidosis (low serum bicarb)
85
hypovolemic shock results from what
dec preload. SV and CO fall when preload dec.
86
features of cardiogenic shock
reduced CI or CO, inc SVR, reduced tissue perfusion
87
treatment of cardiogenic shock
angioplasty, CAGB
88
distributive shock results in what?
results in severe dec in SVR usually with inc CO
89
early septic shocks results in what
dec. SVR, inc CO, resp alkalosis
90
very late septic shock results in what
dec SVR, dec CO, hypotension, metabolic acidosis
91
CVC is used for what
placed in Sup vena cava or RA and used to determine fluid status, not used much
92
arterial cath
provides continuous systemic BP measurement, placed in radial artery
93
treatment choices for shock
dopamine, norepi, epi, phenylephrine, dobutamine, vasopressin
94
in shock where do you want to keep MAP
>60
95
dopamine is used in what type of shock
cardiogenic, raises BP via in SV and HR
96
Dopamine should not be used for what?
acute renal failure
97
Norepi is used when
septic shock when SVR is reduced
98
Phenylephrine is used when
when SVR is reduced and CI is preserved
99
Dobutamine is used when
cardiogenic shock
100
Vasopressin is used when
septic shock esp when catecholamine use proves inadequate
101
definition of HF
complex clinical syndrome that results from any structural or functional impairment of vent filling or ejection of blood
102
cardinal manifestations of HF are what?
SOB and fatigue, and fluid retention
103
LEFT is considered what?
important in classification of patients with HF
104
Normal LVED volume
150ml
105
normal LVES volume
75ml
106
stroke volume normal
75ml, can stay normal until later in the disease because heart can remodel
107
after each hospitalization due to HF what inc
mortality inc. drastically
108
type A HF
risk for develop of LV dysfun
109
type B Hf
asymptomatic LV dysfun
110
type C HF
most typical, symptomatic LV dysfunction
111
Type D HF
refractory LV dysfunction
112
Class 1 is what?
no limitation of physical activity
113
class 2 is what
ordinary physical activity does not cause fatigue, or SOB
114
Class 3 is what
limitation of physical activity, comfortable at rest
115
class 4 is what
symptoms of cardiac insufficiency present at rest, any activity discomfort is dec
116
risk factors for HF
HTN, diabetes, metabolic syndrome, atherosclerotic disease, family cardiomyopathies
117
what are the 2 types of cardiomyopathies
ischemic (CAD caused enough heart death), non ischemic
118
in approaching any patient with CHF what parameters do you need to consider?
congestion (dry or wet), or perfusion (warm or cold)
119
No congestion and not having poor perfusion
warm and dry PCW normal and CI normal
120
no congestion and has poor perfusion
cold and dry PCW low/norm CI dec
121
congestion and not having poor perfusion
warm and wet PCW high and CI norm
122
congestion and has poor perfusion
Cold and wet, PCW elevated and CI dec
123
signs of low cardiac output
cool extremeties, mental status depression, hyponatremia, renal failure, hypo/hypertension
124
pulse pressure should be what
>25%
125
in patients with dyspnea measurement of what is useful to support what?
BNP, useful to support clinical decision making regarding diagnosis of HF
126
meds used for HF
beta blockers, ACEI, diuretics
127
what drug is helpful in HF for blacks
Hydralzine/Isosorbide
128
what is CRT
cardiac rsynch therapy, indicated for patients who have LVEF of 35% or less, causes vent to pace simultaneously
129
patients with refractory HF (advanced) are treated with what?
continuous inotropic infusion, mechanical circulatory support, cardiac transplant, palliative care
130
what are the 3 Rs of lung transplantation
right lungs, right time, right reason
131
what is the number 1 disease process that get lung transplants
COPD, fibrotic patients are surpassing this now
132
Doing less than how many transplants a year causes survival to go down
30
133
What patients are surviving longer from lung transplants
CF patients b/c they are younger
134
donor physiology
disruption of homeostatic regulation, disturbances in endocrine function, intense inflammatory rxn, aspiration
135
Basic lung transplant donor criteria
age <40 pack year smoking history, no sepsis
136
emphysema patients and lung transplants
not really giving them longer life inc quality instead of quantity
137
lung transplant for COPD is under what criteria
FEV1 55, O2 at rest, pulm HTN
138
interstitial lung disease transplant criteria
refer at diagonosis, FVC <20% in 3-6 months
139
what type of lung transplant surgery is usually done
clam shell, can take out both lungs at same time
140
CF transplant criteria
FEV1 50 PO2<55
141
pulm hypertension is what
MAP is greater than 25mmhg at rest and is diagnosed by R heart cath
142
transplant refer
NYHA 3-4 (4 is SOB at rest), RAP >15, mPAP >55 and CI<2
143
transplant workup
blood work, PFTs, CT scans, cancer screening, dentist, R and L heart cath, V/Q scan, pH probe, social work, dietary, financial, transplant surgeon, lung measurements, pulmonary rehab
144
recipients of a transplant need to do what
maintain goal weight BMI 28, enroll in pulm rehanb, maintain pulm rehab, social support
145
what are the goals of immunosurpression
prevent rejection, achieve balance, try to prevent infections
146
Drugs of immunosupr.
Basiliximab and Alemtuzumab is used in induction and usually 3 drugs are used after transplant
147
ECMO
used to treat primary graft dysfunction
148
acute rejection
can be cellular or antibody mediated. cellular is more common
149
antibody rejection is caused by what
antigens in WBC and give immunos drugs and antigens are exposed and body develops antibodies to those antigens and attack lungs
150
how is acute cellular rejection treated
solumedrol is first line, and campath, can be antibody mediated
151
chronic rejection
look to retransplant, BOS/RAS (restrictive allograph syndrome no treatment and very rapid), diagnosis is made by drop in 10-15% in FEV1, treat BOS with roids and Campath
152
ARDS
acute onset, bilateral infiltrates, paO2/FiO2 <200 is ARDS
153
what must be ruled out for the diagnosis of ARDS to be made
cardiac failure and fluid overload
154
mild ARDS
between 200-300
155
moderate ARDS
b.w 100-200
156
severe ARDS
<100
157
ARDS resembles what
acute pulm edema
158
what test are used to rule out pulm edma from ARDS
BNP <100, echo, right heart cath
159
ARDS causes due to direct lung injury
pneumonia, aspiration, pulmonary contusion, fat emboli, near drowning, inhalation injury
160
ARDS causes due to indirect lung injury
sepsis (#1), severe trauma, drug OD, acute pancreatitis, transfusion of blood products (TRALI)
161
signs and symptoms of ARDS
tachypnea, tachycardia, cyanosis, confusion, accessory musc use, hypoxia, acidemia/hypercarbia (in nutshell resp failure)
162
pathophysiology of ARDS
disruption of fluid balance (low protein, change in lymphatics, epithelial and endo cells move apart causing leakage), inflammation (neutrophils and cytokines), and disruption of the coagulation cascade, impairment of gas exchange, dec. lung compliance, pulm HTN
163
Exudative phase of ARDS
1-7 days, hemmorage, interstitial and intra alveolar edema, WBC clump together, Type 1 pneumo and endo cell necrosis, surfactant is lost and replace by hyaline membranes, platelet-fibrin thrombi
164
Proliferative phase of ARDS
7-21 days, fibrosis, fibrosis inside alveoli, chronic inflamm cells, parenchymal necrosis, type 2 pneumo (plays role in repair), arteries and cap shrink up, macrothrombi
165
Fibrotic phase of ARDS
>21 days, honey combing, traction bronchietasis, a lot of fibrosis
166
how do you want to treat ARDS now
keep pPlat pressures <30, high PEEP, low tidal volumes
167
PA vs CV cath in ARDS
no difference in mortality, vent free days, ICU stay, lung or kidney function. PA group had twice as many complications (arrhythmias)
168
what type of fluid strategy is used in ARDS
conservative, improved lung function, shortened MV and ICU stay
169
prone positioning in ARDS
improves V/Q mismatch, inc in end expir lung volume, not study is done on mortality but does improve oxygenation, lateral rotation therapy does not improve oxygenation (helps with VAP)
170
adv methods of MV for ARDS
inverse ratio (cause a raise in PEEP), APRV, BiLevel, PAV
171
ECMO and ARDS
kind of used as a last line treatment, very muddy waters when comes to study
