Resp Final Exam

Front 1

Pulmonary Embolism

Back 1

occlusion of a portion of the pulmonary vascular bed by an embolism: thrombus, tissue fragment, lipids, or air

Front 2

Verchow's Triad

Back 2

risk factors for pulmonary embolism:
1. Venous stasis
2. Vessel injury
3. Hypercoagulability

Front 3

Pulmonary embolism can occur in the following 4 ways

Back 3

1. Massive occlusion
2. Embolism with Infarction
3. Embolism without Infarction
4. Multiple Pulmonary Emboli

Front 4

Neurohumoral substances released d/t Pulmonary Emboli

Back 4

1. Histamine
2. Thromboxane
3. Seratonin

Front 5

3 major S/S of pt with PE

Back 5

1. Hypoxemic
2. Hyperventilation
3. Tachypnic

Front 6

5 effects of Occlusion of part of pulm. circulation

Back 6

1. Hypoxic vasoconstriction
2. decreased surfactant
3. release of neurohumoral substances
4. Pulmonary edema
5. Atelectasis

Front 7

What is the repercussion of Pulmonary HTN?

Back 7

Acute Right Ventricular Heart Failure

Front 8

Pleuritic Pain

Back 8

pain on deep inspiration

Front 9

PE Triad

Back 9

1. Cough
2. Hemoptosis
3. Pleuritic chest pain
- All on Inspiration
- takes hours to days for triad to manifest

Front 10

Why is pt hyperventilating with a
PE

Back 10

b/c J Receptors sense engorged capillaries which makes them dyspnic

Front 11

How to diagnose a PE

Back 11

1. V/Q scan or Pulmonary Angiogram: (most common)

- can also diagnose with CT or MRI

Front 12

Ideal treatment for PE

Back 12

#1 Anticoagulant therapy with IV Heparin or Low Molec Weight Heparin

- Ideal to prevent PE
- Surgical tx: Vena Cava Filter
- Fibrinolytic agent (Streptokinase) for life threatening emboli

Front 13

4 Types of Emboli

Back 13

1. Air
2. Thrombus
3. Fat
4. Amniotic fluid

Front 14

How does a pt get an Air Emboli

Back 14

if the surgical field is 5cm or more above the Right Atrium
(ex. craniotomy)

Front 15

Treatment for Air Embolism

Back 15

Evacuate air from central line
Right side up

Front 16

5 Changes suggestive of PE during anesthesia to look for

Back 16

1. Unexplained arterial hypoemia
2. Hypotension (b/c flow blocked)
3. Tachycardia (decreased preload, C.O. and increased HR)
4. Bronchospasm (b/c release of neurohumoral substances)
5. Decreased End Tidal CO2 with increased arterial CO2

Front 17

Pulmonary Hypertension

Back 17

A rise in pulmonary artery pressure of 5-10mmHg above normal
(mean pressure norm = 15-17mmHg)

Front 18

Primary Pulmonary Hypertension

Back 18

The small arteries (arterioles) become narrow or obliterated as a result of hypertrophy of smooth muscle in the vessel walls and formation of fibrous lesions around the vessels. Thus increases resistance and causes pulm HTN

Front 19

Cor Pulmonale

Back 19

Right Ventricular Disease resulting from pulmonary hypertension

Front 20

Secondary Pulmonary Hypertension can occur d/t any resp. or cardio disorder that:

Back 20

1. Increases the volume or pressure of blood entering the pulm arteries or
2. Narrows of obstructs the pulm arteries

Front 21

4 Causes of Secondary Pulmonary Hypertension

Back 21

1. elevated left ventricular filling pressures, as occur in coronary artery disease and mitral valve disease
2. Increased blood flow through the pulm circulation (L to R shunt) as occur with a VSD or PDA
3. Obliteration or destruction of the pulmonary vascular bed by a pulmonary emboli or chronic destruction of the alveolar wall and capillaries (emphysema)
4. Vasoconstriction of the vascular bed, as occurs with hypoxemia, acidosis, or a combo (most common)

Front 22

What is the treatment for Secondary Pulmonary Hypertension past the point of: Increased pulm artery pressure

Back 22

NONE.
Once there is Hypertrophy of the smooth muscle of pulm arteries the disease is chronic and permanent

Front 23

3 most common pulm obstructive diseases

Back 23

1. Asthma
2. COPD
3. Cystic Fibrosis

Front 24

Clinical features of Asthma

Back 24

1. recurrent episodes of chest tightness
2. wheezing
3. breathlessness
4. coughing

-asthma is acute not chronic

Front 25

3 Phase of Asthma

Back 25

1. Early phase: Bronchospasm
2. Late phase rxn: inflammation
3. Airway hyperrespoinsiveness: can last as long as 4 weeks

Front 26

4 Cellular Mechanisms of Asthma

Back 26

1. Mast Cell Activation: cause release of Arachodinic Acid
2. Degranulation with discharge of mediators: degranulation and discharge of mast cells
3. Synthesis of Arachidonic Acid derivatives
4. Release of cytokines

Front 27

Arachadonic Acid is mediated by what?

Back 27

IgE

Front 28

5 Causes of Airway Obstruction in Asthma

Back 28

1. Contraction of bronchial smooth muscle
2. Inflammation of airway
3. Cytokines: released and cause further inflammation
4. Protease Enzymes: brk up epithelia cells
5. Hypersecretion of mucus

- result in V/Q mismatch and hypoxemia

Front 29

3 mechanisms of uneven ventilation

Back 29

1. Parallel = Obstructive Ventilation (ex. Bronchitis)
2. Series (dilation of sml airway) (ex. Emphysema)
3. Collateral (lung units behind completely obstructed airways may receive inspired gas from neighboring units
3.

Front 30

What is a common cause of Asthma in 25% of asthmatics

Back 30

GI Reflux

Front 31

Principle treatments of Asthma

Back 31

1. Bronchodilators
2. Corticosteroids
3. Allergen Avoidance

Front 32

Anesthetic drug associated with Histamine Release

Back 32

Succynilcholine

Front 33

Volatile Anesthetics have what effect that are advantageous to Asthmatics

Back 33

Bronchodilating Properties

Front 34

Most important thing prior to Intubation

Back 34

DEEP ANESTHESIA during intubation and Lidocaine IV will help

Front 35

Biggest danger for Asthmatics

Back 35

ASPIRATION
(especially if have GI reflux)

Front 36

COPD

Back 36

characterized by progressive air flow limitaion

Front 37

clinical features of COPD

Back 37

1. Wheezing
2. Coughing
3. Dyspnea

Front 38

Clinical features of Bronchitis

Back 38

1. Increased mucus production and increase in size and number of mucous glands and goblet cells in airway epithelium
2. mucus produced is thicker and more tneacious than normal
3. Ciliary fxn is impaired, further reducing mucus clearance
4. Bronchial walls become thickened and inflamed
5. Airway collapse occurs early in expiration, gas trapping occurs, leading to V/Q mismatch, hypercapnia, and hypoxemia

Front 39

Emphysema

Back 39

an abnormal permanent enlargement of gas exchanging airways (resp zone) accompanied by destruction of alveolar walls

Front 40

Major Mechanism of airflow limitation in Emphysema is:

Back 40

Loss of Elastic Recoil
(floppy lung)

Front 41

Primary Emphysema is linked to inherited deficiency of

Back 41

Alpha-1 Antitrypsin
Antitrypsin: normally prevents elastic brk down and without it elastin brks down and is replaced with collagen which has less elasticity and recoil which is why small airways close

Front 42

Type A COPD is:

Back 42

Emphysema
(pink puffers)
do not retain CO2

Front 43

Type B COPD is:

Back 43

Bronchitis
(blue bloaters)
Do retain CO2

Front 44

Respiratory Failure in COPD

Back 44

a failure of maintenance of normal arterial blood gas tensions

Front 45

Mechanisms that contribute to respiratory failure

Back 45

1. Ventilatory failure (reduced alveolar ventilation)
2. Venous admixture as a result of pure intrapulmonary shunt or V/Q mismatch

Front 46

Why does administering O2 to a COPD pt cause hypercapnia

Back 46

1. Ventilatory depression by O2 b/c they loose their sensitivity to CO2 and have only a Hypoxic drive
2. Altered V/Q relationship: O2 opens alveoli preventing HPV but also have a low PO2 in vessels causing low V/Q

Front 47

Treatment for COPD

Back 47

1. Stop Smoking
2. Inhaled Bronchodilators
3. Corticosteroids
4. Active management of infective exacerbations
5. Oxygen, Ventilation if required (O2 post-op)

Front 48

Anesthesia Effects on Respiration

Back 48

1. affects the muscles assoc. with resp
2. usually causes obstruction of pharyngeal airway unless measures are taken to keep it open (mask, ETT)
3. interference with normal action of pharyngeal muscles causes obstruction of the pharynx similar to that seen in sleep apnea
4. soft palate falls against the posterior pharyngeal wall, occluding nasopharynx
5. considerable posterior movement of the tongue and epiglottis
6. selective depression of the intercostal muscles
7. diaphragmatic fxn well preserved
8. disturbed resp. muscle action commonly gives rise to paradoxical inspiratory movements (abd muscles tighten during inspiration which inhibits diaphragm from moving down

Front 49

Change in FRC d/t Anesthesia

Back 49

there is 16-20% decrease in FRC during anesthesia with all anesthetics no matter if pt is paralyzed or awake (when supine)
- obese pt's have an even larger decrease in FRC
- FRC immediately reduced on induction, reaches its final value within min, and does not return to normal until hours after anesthetic

Front 50

Causes of Atelectasis during Anesthesia

Back 50

1. Airway closure as a result of decreased FRC
2. Compression Atelectasis (compressing lung)
3. Absorption Atelectasis: (with 100% O2 causes rapid uptake of O2 into blood causing alveoli collapse and in low lung vol.)

Front 51

Anesthesia Effects of Resp Mechanics

Back 51

1. Arterial O2 is impaired in most pt's during general anesthesia with either spontaneous or controlled ventilation
2. degree of impairment is most severe in the elderly, the obese, smokers, and pt's with lung dx
3. the average degree of venous admixture (shunt) under gen anesthesia is 10% (normally = less than 5%)

Front 52

Dead space and shunt in Anesthetized pt

Back 52

Increase in dead space and shunt with anesthesia

- Alveolar dead space of pt under anesthesia is the Total Dead space of an awake pt

Front 53

Physiologic Dead Space (Total dead space) in Awake vs. Anesthetized pt

Back 53

Awake pt = 30% of tidal volume = dead space

Anesthetized pt = 2/3 (66%) of tidal volume = dead space

Front 54

The effects of anesthesia on gas exchange include

Back 54

1. uniformity of vent and perfusion are decreased
2. increased dead space
3. venous admixture is increased (10%)
4. the major differences are btwn the awake and anesthetized state
5. Both PEEP and CPAP reduce shunt but also decrease C.O which reduces mixed venous O2 content
(norm venous O2 = 40%, anesth. venous O2 = 20%)

Front 55

Effects of LIGHT Anesthesia on Breathing

Back 55

Light anesthesia resp pattern may vary from excessive hypervent to breath holding

Front 56

Effects of MODERATE (or increased depth of anesthesia) on breathing

Back 56

increasing depth of anesthesia cause more regular respirations

Front 57

Effects of DEEP Anesthesia on Breathing

Back 57

Out of phase depression of chest wall during inspiration (see-saw) (paroxysmal)

- the deeper the anesthetic or narcotic the less sensitive the pt is to CO2

Front 58

At what level does is the CO2 to activate a stimulus to breath

Back 58

CO2 = 30 cause stimulus to breath

Front 59

Apneic Threshold

Back 59

the PCO2 at which respiration ceases.
- there needs to be a higher CO2 to stimulate breathing with deeper anesthetic levels

Front 60

Control of breathing under Anesthesia and with Surgical Stimulation

Back 60

Surgical stimulation antagonizes the effects of anesthesia on ventilation
- Increase RR with surgical stimulation even if the pt was fully anesthetized prior to stimulation
- CO2 increases and Min. Vent increases with surgical stimulation

Front 61

Effects of SUPINE position and under anesthesia

Back 61

decreases the FRC by 0.5-1 Liter

Front 62

Effects of LATERAL position and under anesthesia

Back 62

1. Better VENTILATION on non-dependent (UPPER) lung
2. Better PERFUSION of the dependent (LOWER) lung

Front 63

Effects of PRONE position and under anesthesia

Back 63

- if the upper chest and pelvis are supported to allow for free movement of the abd. Respiratory Mechanics are MINIMALLY AFFECTED
(V/Q scatter is minimized)

Front 64

Effects of REGIONAL Anesthesia on Pulmonary System

Back 64

1. Effects of RR and O2 level depend on hight of block and degree of sedation
2. No decrease in FRC (except with OB): decrease in Vital Capacity in OB b/c need for accessory muscles

Front 65

Resp Fxn in early postanesthesia

Back 65

1. first few min. of recovery, aleveolar PO2 may be reduced by the elimination of N2O, which dilutes alveolar O2 (diffusion hypoxia) Lasts 5-7 minutes

2. Airway obstruction common potential cause of hypoxia and may be compounded by residual effects of anesthetic agents on vent. control

Front 66

Diffusion Hypoxia

Back 66

when N2O is excreted it leaves the blood and moves into the alveoli competing for room with O2 thus no room for O2 causing a decrease in O2 levels for the first 5-7 min post-anesthesia

Front 67

Late Postop Resp changes

Back 67

1. low lung vol and increased atelectasis
2. effort-dependent lung fxn test
3. sleepy (tend to obstruct)
4. Resp muscle use
5. sputum retention
6. Ineffective cough and deep breathing

- all these contribute to post-op pneumonia
- Resp changes last 2-3 days after Major surgery

Front 68

Decreased FRC is greatest reduced in what type of surgery?

Back 68

Surgery near the diaphragm
- FRC reaches lowest value 1-2 days post-op
- diaphragm changes only improved by thoracic epidural anesthesia which blocks inhibitory reflex of diaphragm

Front 69

What Effects FRC

Back 69

Position
anesthesia
Lung disease

Front 70

What Effects Closing Capacity

Back 70

Age
Lung Disease

Front 71

3 Principles for Induction of an Asthmatic

Back 71

1. block airway reflexes
2. relaxation of airway smooth muscle
3. prevent release of biochemical mediators

Front 72

Why would a post-op pt be hypoxic

Back 72

1. depression of CO2 and O2 drive
2. residual neuromuscular blockade
3. splinting
4. decreased resp rate d/t opiod
5. airway obstruction d/t muscle relaxation

Front 73

Factors assoc with increased Post-Op Pulm Complications

Back 73

1. surgery over 3.5 hrs
2. increased age
3. smoking hx
4. poor nutrition
5. obese
6. lung dx
7. heart disease
8. anesthetic factor
9. surgical factor

Front 74

Define Obese

Back 74

a BMI greater than 28 or weight more than 20% ideal body weight

Front 75

best place to listen to breath sounds on an obese pt

Back 75

Axilla

Front 76

What does Obesity hypoventilation syndrome iinclude

Back 76

1. loss of CO2 drive
2. sleep apnea
3. hypresomnolence
4. airway difficulty

Front 77

What does Pickwickian Syndrome Include and who gets it

Back 77

Obses pt's get it and includes:
1. More sever hypercarbia
2. sleep apnea and hypersomnolence
3. Low O2
4. Polycythemia
5. Pulm HTN
6. Biventricular failure

Front 78

what percentage of obese pt's are difficult to intubate

Back 78

13%

Front 79

factors that affect DO2 (delivery of O2)

Back 79

1. Flow (C.O.)
2. O2 content (mainly Hgb level)

Front 80

Normal DO2 level

Back 80

1000

Front 81

DO2 equation

Back 81

DO2 = Q (CaO2 x 10)

Front 82

CaO2 equation

Back 82

CaO2 = (1.37 x hgb x SpO2) + (PaO2 x 0.003)