Exam 3 Flashcards
1
Q
primary function of the lungs
A
gas exchange
-O2 transported to tissues
-CO2 transported out of body
2
Q
alveoli
A
-grapelike clusters of air filled sacs
-gas exchange of oxygen and carbon dioxide
-good ventilation
3
Q
ventilation
A
movement of air into and throughout the lungs (inspiration and expiration)
-needs openings in pulmonary airways
4
Q
perfusion
A
movement of blood through pulmonary circulation eventually providing oxygen to every part of the body
5
Q
diffusion
A
-movement gas from high to low concentration
-oxygen diffused out of alveoli into blood
-CO2 diffusion out of blood into alveoli
6
Q
upper airway structures
A
nasopharynx, oropharynx, laryngopharynx
7
Q
lower airway structures
A
Larynx
Trachea
Bronchi
Bronchopulmonary segments
Bronchioles
8
Q
bronchopulmonary segments (right lung)
A
-upper lobe
-middle lobe
-lower lobe
9
Q
bronchopulmonary segments (left lung)
A
-upper lobe
-lower lobe
10
Q
right and left main bronchus difference
A
-right is straighter than left
-makes right lung more susceptible to aspiration and intubation
11
Q
Role of cilia in respiratory tract
A
-push things out airway
-line trachea and bronchi
-defense
-cough reflex
12
Q
what impairs the function of cilia in respiratory tract
A
-smoking
-increased mucous
-alcohol (ethanol)
-temp changes
-low humidity
13
Q
accessory muscles of respiration
A
-sternocleidomastoid
-scalene
-trapezius
-pectoralis major
-internal intercostals
-abdominal muscles
14
Q
when are accessory muscles of respiration active
A
assist the primary muscles when the chest is not expanding or contracting effectively to meet ventilation demands
15
Q
bronchial artery system
A
Supplies oxygenated blood to lungs and pleura
16
Q
pulmonary artery system
A
Vast network of capillary that allows for gas exchange
17
Q
pulmonary artery leaves
A
right ventricle with unoxygenated blood to the lungs
18
Q
pulmonary vein carries
A
oxygenated blood from lungs back into heart
19
Q
how is ventilation controlled
A
-medulla oblongota!
-pons
-“respiratory center” of brain moves air throughout lungs to capillaries
20
Q
proprioreceptors in the muscles
A
-respond to body movement
-stimulated by exercise, respiratory rate and depth increase
21
Q
stretch receptors in bronchi and bronchioles
A
-dilate alveoli
-prevents overstretch
-neonates
22
Q
chemoreceptors in the brain respond to changes in
A
CO2 and pH in bloodstream and cause alterations in the rate and depth of respirations
23
Q
baroreceptors in vascular system respond to changes in
A
blood pressure
-BP decreased, breathe faster
24
Q
how is perfusion controlled
A
-blood flow to alveoli
-affected by gravity: goes to lowest point
25
uneven distribution in perfusion
-body position: sit upright for even distribution
-exercise
-lung zones
-low volume
26
factors affecting perfusion
-fluid volume within lung
-fluid shifts
-interstitial edema
-alveolar edema
27
pulmonary capillary network
-low pressure system
-wrap alveoli
-normal pressure: 22/8 to 25/8 mm Hg
28
pulmonary blood flow zone 1
minimal perfusion
-apex
29
pulmonary blood flow zone 2
intermittent perfusion
-pulmonary artery
-pulmonary vein
30
pulmonary blood flow zone 3
continual perfusion
-most gas exchange
-base
31
ventilation/perfusion ratio (V/Q ratio)
adequate volume air matched with adequate blood flow
-amount of air reaching the alveoli to the amount of blood reaching the alveoli
32
normal ventilation (VA)
4L/min alveolar air flow
33
normal perfusion (Q)
5L/min capillary blood flow
34
normal VA/Q ratio
0.8
-amount air (min)/ amount blood (min)
35
high V/Q ratio
-#1 cause pulmonary embolism
-ventilated but not perfused
-pulmonary embolus!
36
low V/Q ratio (hypoxemia)
-perfused but not ventilated
-airway constriction
-asthma!
-pneumonia!
37
shunt V/Q ratio
-no gas exchange, oxygen and blood not connecting
-no ventilation
-alveolar collapse
-acute respiratory failure!
38
how does oxygen get from environment to tissues
-dissolved in plasma (PaO2)
-bind to hemoglobin (SaO2)
39
oxygen binds to hemoglobin (SaO2)
-affinity in lungs binds O2 to hemoglobin
-affinity in tissues releases O2 at site
-95-100 hemoglobin should be saturated!
40
oxyhemoglobin dissociation curve: PaO2
partial pressure of oxygen in arterial blood
-80-100 mm/Hg!
41
oxyhemoglobin dissociation curve: SaO2
saturation of hemoglobin with oxygen in arterial blood
-95-100%
42
what causes right shift of oxyhemoglobin curve
-increased hydrogen, decreased pH: acidosis!
-increased Co2!
-increased temp!
43
what does right shift of oxyhemoglobin curve do to oxygen saturation and availability
-enhances O2 release to tissues
-less affinity
-oxygen less tightly bound to hemoglobin
44
what causes left shift of oxyhemoglobin curve
-decreased hydrogen, increased pH: alkalosis!
-decreased Co2!
-decreased temp!
45
what does left shift of oxyhemoglobin curve do to oxygen saturation and availability
-decreases O2 release to tissues
-hemoglobin holds on longer to oxygen
46
hypoventilation
-not enough air in
-insufficient air delivery to alveoli causes inadequate O2 delivery and Co2 removal
47
hypoventilation causes
-medication
-obesity
-pain
-sleep apnea
-paralysis
-pt out of surgery at risk
48
hyperventilation
-breathe too fast
-increased air entering alveoli resulting in hypocapnia (PaCo2 below 35)
49
hyperventilation causes
-hypoxic stimulation
-anxiety
-fear
-fever
-sepsis
-brain stem injury
50
hypoxia
-oxygen at tissue level
-low O2 in tissues
-cant measure
-pale, blue lips and fingernails
51
hypoxemia
-not enough oxygen in bloodstream
-low hemoglobin saturation
-measure with pulse ox (SaO2)
52
normal PaO2
80-100
53
mild hypoxemia PaO2
70-79
54
moderate hypoxemia PaO2
60-69
55
severe hypoxemia PaO2
<60
56
acute respiratory failure
disturbed gas exchange resulting in abnormal blood gas values (ABGs)
-failure of oxygenation (hypoxemia) or failure of ventilation (hypercapnia) or both
-pulmonary system fails to oxygenate the blood or fails to eliminate carbon dioxide
57
normal ABGs
-PaO2: 80-100
-PaCo2: 35-45
-pH: 7.35-7.45
58
how is acute respiratory failure diagnosed
ABGs
-PaO2: < 60 (hypoxemia)
-PaCo2: >50 (hypercapnia)
-pH: < 7.3
CXR
59
acute respiratory failure general features
-headache
-dyspnea
-confusion!
-restlessness/agitation!
-dizziness
-tremors
60
early signs and symptoms of acute respiratory failure
-rapid shallow breathing
-increased inspiratory muscle movement
61
late signs and symptoms of acute respiratory failure
-cyanosis
-nasal flaring
-sternal/intercostal retractions
-cool clammy skin
-dysrhythmias
-decreased capillary refill
62
acute respiratory failure treatment
-ventilatory support
-airway patency
-supportive care (keep all other organ systems functioning)
-nutrition
-pain management
-emotional support
63
pulmonary hypertension etiology
-pulmonary vasculature is high flow, low pressure system
-sustained pulmonary arterial pressure >30 mmHG
64
primary pulmonary hypertension (PPH) etiology
-rapidly progressive/poor prognosis (only live few years)
-no underlying cause just happens
65
secondary pulmonary hypertension
-get from HF or chronic lung disease
-increased pulmonary blood flow (left sided failure)
-increased resistance to blood flow (hypoxic responsive vasoconstriction)
-increased left atrial pressure (aortic stenosis)
-live longer
66
pulmonary hypertension pathogenesis
over time right sided heart failure occurs
67
pulmonary hypertension signs and symptoms
-often asymptomatic until damage is done
-exercise intolerance is first symptom!
-chest pain
-hemoptysis (cough up blood)
-pulmonary edema
-cor pulmonale: right sided heart enlargement/failure
68
pulmonary hypertension diagnosis
-pulmonary artery catheter measurement
-CXR: pulmonary arteries and right ventricle enlargement
-EKG
-echo
69
pulmonary hypertension treatment
-control underlying disease process
-oxygen
-vasodilators/diuretics!
-lung or heart transplant: not common
70
Virchow's triad
factors that predispose thrombus formation
-venous stasis
-hypercoagulability
-damage to vessel wall
71
pulmonary venous thromboembolism etiology
-blood clot lodges in vascular space
-occludes pulmonary vasculature
72
pulmonary venous thromboembolism sources
-deep veins legs (90%)
-fat emboli
-air emboli
-amniotic fluid: delivery
-foreign material
-septic bodies
73
pulmonary thromboembolism risk factors
-immobility
-trauma
-pregnancy
-cancer
-heart failure
-estrogen use (birth control)
74
pulmonary thromboembolism pathogenesis
-thrombus dislodged from trauma, exercise and muscle action, change in blood flow pattern
-travel to heart and lungs
75
pulmonary thromboembolism signs and symptoms
-restlessness
-anxiety
-sense of "impending doom"
-dyspnea
-tachycardia
-chest pain
76
pulmonary thromboembolism diagnosis
-Va/Q lung scan
-pulmonary arteriography: inject dye into pulmonary artery
-ultrasound lower extremities
77
pulmonary thromboembolism treatment
-prevention: nurses role, range of motion, SCDs
-heparin therapy
-vena cava filter: wire traps clot
-embolectomy: surgically remove embolus
78
lung cancer etiology
-85% smoking
-asbestos exposure
-over age 50
79
lung cancer four major types
-squamous cell
-adenocarcinoma
-large cell
-small cell (oat cell)
80
lung cancer pathogenesis squamous cell
-detected in sputum
-detected early
81
lung cancer adenocarcinoma and large cell carcinoma pathogenesis
metastasize to distant organs
82
lung cancer small cell carcinoma (oat cell) pathogenesis
-rapid growth
-widespread metastasis
-most difficult to treat
83
lung cancer signs and symptoms intrathoracic
lung and airway
-dyspnea
-cough
-increased sputum
-hoarseness
-hemoptysis
-chest pain
84
lung cancer signs and symptoms extrathoracic
non airway
-weight loss
-anemia
-facial/ upper extremity edema: retain fluid, prevents blood flow down body
85
lung cancer diagnosis
-bronchoscopy washings: tube takes out tx
-pleural fluid samples
-biopsy
-CXR
86
lung cancer treatment
surgery, radiation, chemotherapy
87
asthma etiology
-episodic airway obstruction resulting from bronchospasm, increased mucus, mucosal edema, usually reversible with bronchodilators
-inflammatory chemicals from mast cells
88
Asthma triggers
-allergens
-stimuli
-twice as many boys
89
Intrinsic/Environmental (Non-Allergic) asthma
-middle age, poorer prognosis
-precipitated by respiratory infections and exercise
-stress
-pulmonary irritants
-foods
-drugs
90
Extrinsic/Genetic (Allergic) IgE mediated asthma
-begins in childhood
-family history
-sensitivity to specific allergens: pollen, animal dander, dust etc
91
asthma pathogenesis
-mediated by IgE after exposure to specific antigen
-inflammation: bronchospasm, mucosal edema, mucous plug formation, airway remodeling (scarring)
-changes in epithelial cells
-genetic
-seasonal, environmental, occupational factors
-can lead to COPD
92
asthma signs and symptoms
-wheezing! airway constriction
-chest tightness
-dyspnea
-cough
93
asthma diagnosis
-pulmonary function tests
-ABGs: CO2 and O2 values
-CXR
-sputum exam
94
asthma treatment
-avoid triggers
-bronchodilators
-steroids
-oxygen
95
acute bronchitis etiology
-acute inflammation of trachea and bronchi from bacterial or viral infection
-smokers, young children, elderly, winter, bacterial infections, smoking
96
acute bronchitis pathogenesis
-airway becomes inflamed/narrowed by excessive mucous secretion
-swelling from exudative fluid
97
acute bronchitis signs and symptoms
-fever
-cough
-malaise
-sore throat
-post nasal drip
98
acute bronchitis diagnosis
-acute cough (symptomology)
-purulent sputum
-elevated WBC
99
acute bronchitis treatment
-cough medicine
-self limiting: caused by virus
-antibiotics if bacterial
100
chronic bronchitis- type B COPD etiology
combination of chronic bronchitis, emphysema and reactive airway disease (RAD)
-increased mucous production
-chronic cough
-blue bloater: difficulty air in (blue) fluid backs up from edema (bloater) !
101
chronic bronchitis- type B COPD pathogenesis
-chronic inflammation of bronchial mucosa
scarring
-mucous plugs
-decrease arterial oxygen, airflow limitation
102
chronic bronchitis- type B COPD signs and symptoms
-chronic cough
-barrel chest
-overweight
-excess body fluids
-DOE
-muscle aches
-end stage: right heart failure
103
chronic bronchitis- type B COPD diagnosis
-hypersecretion bronchial mucous
-chronic cough
104
chronic bronchitis- type B COPD treatment
-prevent flareups
-limit disease progression
-bronchodilators!
-corticosteroids!
105
emphysema- type A COPD etiology
destructive changes of alveolar wall without fibrosis or dilation!
-alveolar wall breaks down and loses area to gas exchange
106
emphysema- type A COPD causes
-smoking
-air pollution
-occupational hazards
-alpha 1 antitrypsin deficiency (smoking causes)!
107
emphysema- type A COPD pathogenesis
-release proteolytic enzymes from inflammatory cells
-smoking inactivates alpha 1 antitrypsin
-breakdown of alveolar walls
108
loss of alveolar wall in emphysema
-decreased capillary beds for gas exchange
-less elasticity lung tissue
-decreased air flow
-air trapping in alveoli
109
emphysema- type A COPD signs and symptoms
-accessory muscles
-pursed lip breathing!
-leaning forward to breathe
-pink puffer (vasodilated)
-barrel chest
-clubbing
110
emphysema- type A COPD treatment
-prevent flareups
-limit disease progression
-bronchodilators!
-corticosteroids!
111
bronchiectasis etiology
misshaped alveoli, retain sputum which gets thick and cant cough out
-classified by shape: saccular, cylindrical, fusiform
112
bronchiectasis pathogenesis
-dilation bronchioles
-bronchiole wall destruction
-purulent secretions lead to airway obstruction!
113
bronchiectasis signs and symptoms
-chronic cough
-copious foul smelling, green or yellow sputum!
-fever
-pallor
-clubbing
114
bronchiectasis treatment
Antibiotics
Bronchodilators
Chest physiotherapy
Nutrition
115
cystic fibrosis etiology
-autosomal recessive disorder!
-cant retain sodium
-hyperthick mucous secretions
116
cystic fibrosis pathogenesis
-CFTR on chromosome 7
-thick secretions plug glands and ducts: pancreas, enzymes break down food which you dont have so youre very thin.
117
cystic fibrosis bronchopulmonary system
Airway obstruction
Stasis of secretions
Frequent infections
Atelectesis
Air trapping
118
cystic fibrosis signs and symptoms
-violent cough with thick sticky sputum
-recurrent pulmonary infections
-bronchitis
-right sided heart failure (cor pulmonale)
119
cystic fibrosis physical exam signs
-clubbing
-dyspnea
-sternal retractions
-hyperresonance
-adventitious breath sounds
-growth rate, weight, head circumference
120
cystic fibrosis treatment
-150% caloric intake
-high protein
-replacement pancreatic enzymes
-aggressive management of pulmonary infections: leading cause of death!
121
interstitial lung disease etiology
Infiltration of the alveolar walls by cells, fluid, & CT
-scarred lung tx, lungs dont expand and recoil
122
interstitial lung disease pathogenesis
-not well understood
-3 pathologic patterns: inflammation, fibrosis, destruction
123
interstitial lung disease signs and symptoms
-progressive dyspnea
-non productive cough
124
interstitial lung disease diagnosis
-pulmonary functions tests
-honeycomb CXR
125
interstitial lung disease treatment
Remove environmental triggers (smoking)
Immunosuppressive therapy
Steroids
Lung transplant in selected patients
126
acute respiratory distress syndrome (ARDS) etiology
-damage to alveolar capillary membrane
-hallmark: hypoxemia refractory to increasing levels of supplemental O2, cant get person saturated with oxygen!
127
acute respiratory distress syndrome (ARDS) is associated with
-trauma
-shock
-sepsis
128
ARDS memory jogger
A-assault to the pulmonary system
R-respiratory distress
D-decreased lung compliance
S-severe respiratory failure
129
acute respiratory distress syndrome (ARDS) pathogenesis
widespread inflammation leads to
-pulmonary edema
-atelectasis (collapsing alveoli)
-fibrosis causes lungs to stiffen
130
acute respiratory distress syndrome (ARDS) signs and symptoms
-precipitating event 1-2 days prior
-increase HR, RR
-shallow rapid breathing
-crackles, wheezing
CXR changes late!
131
acute respiratory distress syndrome (ARDS) diagnosis
-tell tale sign is CXR initially normal but progressing to "whiteout"
132
acute respiratory distress syndrome (ARDS) treatment
-high pressure ventilation (PEEP)
-treat underlying cause
-supportive care
133
Common cold/rhinitis etiology
viral infection of upper respiratory system
-caused by rhinovirus, parainfluenza virus, respiratory virus, coronavirus, adenovirus
-acquire immunity
-portal of entry: nasal mucosa and conjunctiva
134
Common cold/rhinitis signs and symptoms
-increased nasal secretions
-lacrimation
-swelling and redness respiratory tract
-sore throat
-hoarseness
-headache, fever, chills
135
Are antibiotics a good treatment for rhinitis
antibiotics are ineffective because its a virus
136
rhinosinusitis/sinusitis etiology
-inflammation of paranasal sinuses
-blockage and narrowing of ostia that drain sinuses
137
rhinosinusitis/sinusitis predisposing risks
-URI
-nasal polyps
-barotrauma (tissue damage)
-swimming
-abuse nasal sprays
138
rhinosinusitis/sinusitis signs and symptoms
facial pain and headaches
139
rhinosinusitis/sinusitis diagnosis and treatment
diagnosis: visual inspection and palpation, sinus xray
treatment: antibiotics if bacterial, decongestants, antihistamines, saline sprays, heated mist
140
pneumonia etiology
inflammation in alveoli and interstitium of lungs
-occurs as result of: aspiration, inhalation, translocation (microorganisms escapes)!
141
pneumonia classifications
-Community acquired vs Hospital acquired
-Bacterial vs atypical vs viral
-Bacterial
-Gram + vs gram -
-Opportunistic in immunocompromised patients
142
pneumonia risk factors
elderly, immunocompromised, immobility, chronic illness
143
pneumonia pathophysiology
-entry of microbes in lungs then inflammatory response in lungs
144
inflammatory response in lungs with pneumonia
-exudate collects and thickens in alveoli and interstitium
-V/Q mismatch
-bacteria produce toxins worsening injury
145
pneumonia signs and symptoms
-fever/chills
-crackles
-wheeze
-rales
-cough
-coryza: cold S&S
-headache
-malaise
146
pneumonia diagnosis
-CXR
-sputum cultures and gram stain
-increased WBC count
147
pneumonia treatment
antibiotics if bacterial, hydration, S&S relief
148
tuberculosis initial infections
immunocompromised, malnourished, overcrowded
149
tuberculosis signs and symptoms
-low grade fever
-night sweats
-chronic progressively productive cough
^^ tell tale signs
150
tuberculosis pathophysiology
-caused by mycobacterium tuberculosis
-airborne
-may affect lungs and lymphatics
-Ghon complexes: hard to get antibiotics through this !
151
tuberculosis diagnosis
-3 consecutive am sputum cultures
-CXR
-mantoux (skin test)
152
tuberculosis treatment
-multidrug therapy for 9-12 months
-2-4 weeks isolation
-compliance!
153
pleural effusion, pneumothorax, and hemothorax
accumulation of fluid or air in the pleural space
154
pleural effusion
-collection of fluid or pus in pleural space
-transudative, exudative, empyema
155
pleural effusion type (chylothorax)
collection of chylous (lymph fluid) usually associate with local infection
156
pleural effusion type (hemothorax)
collection of blood
157
pleural effusion pathophysiology
-changes in hydrostatic and oncotic pressure in pleural capillary and intrapleural
-increased pleural membrane permeability
-impaired lymphatic drainage
158
pleural effusion signs and symptoms
-may be asymptomatic
-dyspnea
-pain worsens with inspiration
-decreased chest movement, breath sounds and fremitus
159
pleural effusion diagnosis and treatment
-thoracentesis: remove fluid
-drains
-fluid analysis
-imaging
160
pneumothorax
air in pleural space
161
primary pneumothorax
thin, tall
20-40 yo males,
cigarette smokers
Generally occur in the apices (upper 1/3) of the lung as a result of negative pressure created during inspiration.
Smaller airways collapse leaving compressed lung and air space
162
secondary pneumothorax
Underlying lung disease leads to weakened small airways which collapse with respirations.
163
traumatic pneumothorax
penetrating trauma, air enters pleural space through chest wall collapsing lung
164
tension pneumothorax
trapped air in pleural space
-major life threatening complication: mediastinal shift of heart and trachea to contralateral side
165
pneumothorax signs and symptoms
-decreased or absent breath sounds
-hyperresonance
-dyspnea
-increased RR with respiratory alkalosis
166
Pneumothroax treatment
-chest tube
-pleurodesis
167
hemothorax etiology
collection of blood in plural space
168
hemothorax signs and symptoms
-decreased or absent breath sounds
-hyperresonance
-dyspnea
-increased RR with respiratory alkalosis
-decreased RBC count!
169
hemothroax treatment
chest tube, surgical correction, blood replacement
170
what is pH
-reflects hydrogen ion concentration!
-degree of acidity or alkalinity
171
if pH is abnormal
cellular function is impaired
-death below 6.9 or above 7.8
172
acid
-increase hydrogen, decrease pH
173
alkaline (base)
-decrease hydrogen, increase pH
174
type of acid our bodies make during normal cellular metabolism
-carbonic acid
-metabolic acid
175
carbonic acid
Co2 and H2O make H2CO3 (carbonic acid) , get rid through respiratory system
176
metabolic acid
kidney regulated
-becomes lactic acid
-ex: anaerobic metabolism
177
buffers
-first line of defense
-immediate
-chemicals control pH
-keeps 20:1 bicarbonate to Co2
178
bicarbonate buffer
-most important in extracellular fluid!
-HCO3- (weak base) bicarbonate
-H2CO3 (weak acid) carbonic
179
too much acid in bicarbonate buffer
bicarbonate takes up released H and become carbonic acid, excreted through respiratory system
180
too little acid in bicarbonate buffer
bicarbonate releases H
181
respiratory system
-second line of defense
-Co2 and h20 make carbonic acid (H2CO3)
182
what kind of acid do the lungs excrete
carbonic acid and water
183
what is the indicator of lung effectiveness
PaCo2
184
what do the lungs do if the Co2 is high?
hyperventilate, rate and depth increase and "blow off" CO2
-PaCo2 high means carbonic acid accumulated in blood
185
what do the lungs do if the Co2 is low?
hypoventilation, rate and depth decrease
-retain carbonic acid (Co2) because not enough
186
renal system
3rd line of defense
-excrete any acid except carbonic acid
-excrete or retain H
-excrete or retain HCo3 (bicarbonate)
187
kidneys excrete H if
too acidic (low pH)
188
kidneys retain H if
too basic (high pH)
189
kidneys retain HCo3 (bicarbonate) if
too acidic
190
kidneys excrete HCo3 (bicarbonate) if
too basic
191
what is the indicator of renal effectiveness
HCo3 (bicarbonate)
192
how do the lungs compensate for the kidneys?
compensate for acid imbalances of metabolic acids
-get rid of or add carbonic acid to balance kidneys metabolic acids
193
how do the kidneys compensate for the lungs?
compensate for acid imbalances of carbonic acids
-get rid of or add metabolic acids to balance lungs carbonic acid
194
if compensation has been achieved
pH is within 7.35-7.45
195
respiratory acidosis
caused by hypoventilation!
-excess carbonic acid (high PaCo2): hypercapnia
196
respiratory acidosis etiology
-COPD Pulmonary edema
-Pneumonia
-Airway obstruction
-Underventilation on vent
-Hypoventilation
-Anesthetic, sedatives, narc overdose
-Neuromuscular disorders
-Severe spinal deformities
-CNS depression
-Cardiopulmonary arrest
197
respiratory acidosis clinal manifestations
-hypercapnia
-anxiety
-restlessness
-headache
-lethargic
-fatigue
-SOB
-tachypnea
-cough
-dysrhythmias (hyperkalemia)
-advanced: confusion, somnolence. coma
198
what system compensates for respiratory acidosis
-increased renal excretion of H and retention of HCO3- (bicarbonate)
199
respiratory acidosis treatment
improve ventilation
-oxygen
-bronchodilation
-treat infection
200
respiratory alkalosis
hyperventilation!
-carbonic acid deficit (low Co2): hypocapnia
-increased respiratory acid excretion (RR>20)
201
respiratory alkalosis etiology
-lung disease with SOB
-overventilation on vent
-acute pain
-anxiety
-prolonged sobbing
-alcohol intoxication
-stimulation of brain stem
202
respiratory alkalosis clinical manifestations
-hypocapnia
-increased neuromuscular excitability: hypocalcemia and hypokalemia
-cerebral vasoconstriction
203
what system compensates for respiratory alkalosis
-decreased renal excretion of H and increased excretion of HCO3- (bicarbonate)
204
respiratory alkalosis treatment
identify underlying trigger
-pain management
-breathe in paper bag
205
metabolic acidosis
excess any acid except carbonic acid (H2CO3) or decrease in base or combination of both
206
metabolic acidosis etiology
-ketoacidosis
-lactic acidosis
-fistulas
-electrolyte imbalance
-kidney disease
-decreased base: assidosis (diarrhea)
207
metabolic acidosis clinical manifestations
-neuromuscular fatigue
-confusion
-drowsiness
-twitching
-respiratory distress
-nausea and vomiting
-hyperkalemia
-tachycardia
208
what system helps compensate for metabolic acidosis
respiratory hyperventilation
-increased rate and depth
209
metabolic acidosis treatment
correct underlying disorder
210
what potassium imbalance happens with acidosis
too much hydrogen causing hyperkalemia
-need to kick out potassium
211
metabolic alkalosis
deficit of any acid besides carbonic acid or an increase in base or combination
212
metabolic alkalosis etiology
decreased metabolic acid:
-emesis
-gastric suction
-increased renal secretion
-hypokalemia
increased base (bicarbonate):
-antacids
-transfusion
-excess IV sodium bicarbonate
213
metabolic alkalosis clinical manifestations
-hypotension
-hypokalemia: muscle spasms and weakness
-hypocalcemia: Chvosteks sign (face twitches with touch), Trousseaus sign (hand twitches with blown up BP cuff)
214
what system helps compensate for metabolic alkalosis
respiratory hypoventilation
215
metabolic alkalosis treatment
electrolyte and fluid replacement
216
alkalosis causes
hypokalemia
217
pH normal range
7.35-7.45
218
pH 7.4 or below
acidosis
219
pH 7.41 or above
alkalosis
220
PaCO2 normal value
-35-45 mm/Hg
221
HCO3 (bicarbonate)normal value
22-26 mEq/L
222
PaCO2 less than 35 pH
alkalosis (base)
223
PaCO2 greater than 45 pH
acidosis (acid)
224
HCO3 less than 22 pH
acidosis (acid)
225
HCO3 greater than 26 pH
alkalosis (base)
