Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Coexisting > Respiratory Diseases > Flashcards

Respiratory Diseases Flashcards

1
Q

Breathing Mechanics

What happens in inspiration?

A
  • Active contraction of diaphrarm: 75 % of inspiration
  • External intercostal muscles: 25 % of inspiration
  • Other muscles assist during respiratory compromise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Breathing Mechanics

What happens in expiration?

A
  • Passive recoil of ribcage
  • Forced expiration: Internal intercostals and abdominal muscles
    • Pursed lip breathing seen in COPD patients (autopeeping)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Accute Upper Respiratory Tract Infection

statistics

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Management of Anesthesia for URI

How many weeks before its safe to give anesthesia?

How many weeks for hyper-reactive airways?

what gets decreased by GA?

What can PPV do to infection?

A
  • 4 weeks post -URI safe to give anesthesia
  • 6 weeks or more for hyper-reactive airways
  • Trachial mucociliary flow and pulm bactericidal activity is decreased by GA
  • PPV may force infection deeper into lungs
  • Immune response is already altered by surgery and anesthesia

*****cancel case if it has been a shorter period of time***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PeriOperative care of URI

A
  • Regional and peripheral nerve block are great technique
  • pulmonary toilet – cough and deep breathe
  • recent hx of URI symptom is extremely important
  • We also need to know patients travel experience
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Coronaviruses

definition

what is “spill over” event

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

SARS- CoV -2

What are the common signs and symptoms?

What happens in severe cases?

A

Prevention

  • hand washing, covering sneezing or coughing, avoid contact with people with symptoms of respiratory illness

treatment:

supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are Intrisic Lung Diseases?

A

These Diseases causes either:

  • Inflammation and /or scarring of lung tissue
  • Fill the air spaces with exudate and debris

Asthma, COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are Extrinsic Lung Diseases?

A

Diseases involving the chest wall, pleura, and respiratory muscles (respiratory pump) [excursion and inhalation]

  • disorders of these structures will cause lung restriction and ventilatory dysfunction
  • non- muscular disease of the chest wall
  • neuro- muscular disorders (polio)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Obstructive Lung Disease

Asthma is what kind of flow obstruction?

A

Asthma: chronic airway inflammation and reversible expiratory flow obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What question do we ask patients with Asthma upon assessment?

A
  • How do they look
  • How do they sound?
  • What are they telling you? [believe when they say their lungs are tight]
  • Have they received treatment? Did it help?
  • Have they been in this condition in the past? what happened? what made them improve?

—> what are your triggers?

–> when was your last attack?

–> how often do you take your medications?

–> have you been to the ER because of asthma?

–> have you ever been admitted to the hospital because of asthma?

–> have you ever had a breathing tube placed because of asthma?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Spirometric Parameters

Define: Forced expiratory volume in 1 seconf (FEV1)

A

Volume of air that can be forcefully exhaled in 1 second (80 % - 120% of predicted value = normal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Spirometric Parameters

Forced Vital Capacity

A

The max amount of air that can be expelled after deep inhalation (~3.7 L in females, ~ 4.8 L in males)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Spirometric Parameters

Ratio of FEV1 to FVC

A

75% - 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Spirometric Parameters

Forced expiratory flow @ 25% - 75% of vital capacity (FEF25%-75%) Aka Maximim mild-expiratory flow, MMEF)

A

Measurement of flow through midpoint of forced expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Spirometric Parameters

Maximum voluntary ventilation (MVV)

A

measured over 15 seconds (males 140-180 L/min, females 80-120 L/ min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Asthma Findings

What will you see when your patients is having a marked asthma attack?

A

FEV<strong>1 </strong>(% predicted)= 35 -49

FEF <strong>25%-75%</strong> (% predicted) = 30 - 40

PaO2 (mmHg) = <60

PaCO2 = >50 [hypercarbia]

look at severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Respiratory Flow Volume Curves

A

Obstructive = problem with exhalation

Restrictive disease: problems with inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of Asthma

what are controllers and what are relievers?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

This is an absolute emergency ( status asthmaticus)

What are the treatments?

Turbutaline and Epi dose

A

Turbutaline dose: 250 mcg Sub Q

Epi : 400 mcg sub Q

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Asthma Management

What type of ventilation?

A

GA max bronchodilation

VA is also good for bronchodilation

SEVO is a really good thing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the goal of preoperative assessment of Asthma?

A

Goal is to formulate anesthetic plan that prevents or blunts expiratory airway obstruction

  • Severity and characteristics of their disease
  • General appearance of patient
  • Auscultation of lung sounds
  • Eosinophil count
  • PFTs
    • FEV1 before and after bronchodilator use
    • Decrease in FEV1 OR FVC of <70% and FEV1/FVC ratio <65% of predicted values – may indicate risk factor for peri-op complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PreOperative Care for Asthma

A
  • CPT, pulmonary toilet, antibiotics, bronchodilator therapy
  • Measurement of blood gasses
  • Continue antiinflammatory and bronchodilator therapy
  • consider stress-dose steroids
  • Ideally, free of wheezing and peak expiratory flow >80 % of predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Chronic Obstructive Pulmonary Disease?

A

COPD is a disease of progressive loss of alveolar tissue and progressive airlow obstruction that is not reversible. Pulmonary elastic recoil is lost as a result of bronchiolar and alveolar destruction, often from inhaling toxic chemicals such as are contained in cigarette smoke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

COPD

Risk Factors

S/S

Diagnosis

A

COPD include

(1) cigarette smoking,
(2) occupational exposure to dust and chemicals, especially in coal mining, gold mining, and the textile industry,
(3) indoor and outdoor pollution,
(4) recurrent childhood respiratory infections, and
(5) low birth weight. α1-Antitrypsin deiciency is an inherited disorder associated with premature development of COPD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Treatment of COPD

A

Smoking cessation and long-term oxygen administration are the two important therapeutic interventions that can alter the natural history of COPD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What s/s are great predictors of postop pulmonary complications

A
  • smoking, diffuse wheezing, productive cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Strategies to decrease Incidence of Postoperative Pulmonary Complications

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are predictors of post-op pulmonary complications in COPD?

A
  • smoking
  • diffuse wheezing
  • productive cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When are PFTs predictive of post-op pulmonary function?

A

they are really not predictive of postOp pulmonary function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When are PFTs useful?

A

useful for obtaining baseline functioning and for post Op evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Management of Anesthesiafor COPD

preOperative

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Intraoperative Managament of COPD

  • is regional anesthesia ok to use?
  • GA
    • What agents would you choose and why?
    • What about maintenance?
    • What about emergence?
    • Is emergence shorter or longer in COPD patients and why?
A
  • Regional Anesthesia
    • Spinal and Epidural is OK; but we need to becareful in administering epinephrine to patients with poor perfusion
  • GA
    • You want to choose medications with rapid elimination (desflurane, sevoflurane)
    • Emergence is longer
    • Be careful with Nitrous
  • Ventilation of Patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do you ventilate patients with COPD?

A

Patients with COPD are at increased risk of lung injury during mechanical ventilation in the perioperative period. The goals of mechanical ventilation must be to avoid dynamic hyperinlation of the lungs and prevent development of auto- PEEP.

  • Most studies show low tidal volumes (6–8 mL/kg), peak airway pressures less than 30 cm H2O, and Fio2 titrated to keep Spo2 greater than 90% result in lower levels of inlammatory markers in bronchoalveolar lavage luid of mechanically ventilated patients. Patients with moderate to severe COPD can have cystic air spaces in the lungs that carry a risk of rupture once positive pressure ventilation is instituted. In patients with COPD who become hemodynamically unstable during mechanical ventilation, the diferential diagnosis must include tension pneumothorax and bronchopleural fistula.
  • SLOW SMOOTH I TIME AND LONE E TIME
35
Q

What is air trapping?

What can happen in air trapping?

A

The phenomenon of air trapping, also called auto PEEP, intrinsic PEEP, or dynamic hyperinlation, occurs when positive pressure ventilation is applied and insufficient expiratory time is allowed.

  • This contributes to increased intrathoracic pressure, impedes venous return, and transmits the elevated intrathoracic pressure to the pulmonary artery. An increase in pulmonary vascular resistance can lead to right ventricular strain. Hyperinlated lungs may exert direct pressure on the heart, limiting its ability to expand fully during diastole even with adequate preload. Shift of the ventricular septum and ventricular interdependence due to the shared pericardium may cause a distended right ventricle to impinge on illing of the let ventricle.
36
Q

Post- Operative Management of COPD

A
37
Q

What causes Bronchiectasis

How is diagnosed?

A

Pathophysiology

Bronchiectasis is characterized by l_ocalized irreversible dilation of bronchi caused by destructive inlammatory processes involving the bronchial wall_.

For example, bacterial or myco bacterial infections can cause inlammation and destruction of medium-sized airways that can eventually lead to airway collapse, airlow obstruction, and an inability to clear secre- tions.

38
Q

What is the pathopgysiology of Cystic Fibrosis (CF)

treatment and diagnosis

A

*** sweat test is a test for CF**

**patients tend to have horrible infections.**

TREATMENT

  • Clearance of airway secretions
  • Bronchodilator therapy
  • Pulmozyme
  • Antibiotic often long term
  • Anesthesia Management:
    • Avoid intubation if possible
    • Volatiles are good
    • O2 is good
    • Humidification is good
39
Q

Other Expiratory Airflow Obstructions

A
40
Q

Tracheal Stenosis

pathophysiology

Diagnosis and treatment

A
  • Post- prolonged endotracheal intubation
  • Tracheal ischemia with circumferential scarring
  • Symptoms if trachea is <5cm in diameter
  • Dyspnea at rest
  • Accesory muscle use
  • Surgical dilatation or surgical resection
41
Q

What are samples of Acute Intrinsic Restrictive Lung Disease (Alveolar
and Interstitial)

A
  • Pulmonary Edema
  • Aspiration
  • Neurogenic Pulmonary Edema
  • Drug-Induced Pulmonary Edema
  • High-Altitude Pulmonary Edema
  • Reexpansion Pulmonary Edema
  • Negative Pressure Pulmonary Edema
42
Q

What are samples of Chronic Intrinsic Restrictive Lung Disease (Intersti-
tial Lung Disease)

A
  • Pulmonary Fibrosis
  • Sarcoidosis
  • Hypersensitivity Pneumonitis
  • Eosinophilic Granuloma
  • Alveolar Proteinosis
  • Lymphangioleiomyomatosis
43
Q

What are samples of Chronic Extrinsic Restrictive Lung Disease

A
  • Thoracic Extrapulmonary Causes
  • Extrathoracic Causes
44
Q

What is the characteristic of Restrictive Lung disease?

What is the hallmark of restrictive lung disease?

A
  • Restrictive lung diseases are characterized by a decrease in all lung volumes, especially total lung capacity (TLC), a decrease in lung compliance, and preservation of expiratory flow rate
  • Restrictive lung diseases affect both lung expansion and lung compliance (ΔV/ΔP).
  • The hallmark of restrictive lung disease is an inability to increase lung volume in proportion to an increase in pressure in the alveoli

These disorders can result from connective tissue diseases, environmental factors and other conditions that lead to pulmonary fibrosis, any conditions that increase alveolar or interstitial fluid, and any conditions that limit appropriate excursion of the chest/ diaphragm during breathing. These conditions lead to a reduction in available surface area for gas difusion, leading to ventilation/perfusion mismatching and hypoxia. Intrinsic or extrinsic pathologies can afect the ability of the lung to expand. As the elasticity of the lungs worsens, patients become symptomatic owing to hypoxia, inability to clear lung secretions, and hypoventilation. This leads to restrictive lung disease manifested by a reduced forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC), with a normal or increased FEV1/FVC ratio and a reduced difusing capacity for carbon monoxide (DLco). However, the principal feature of these diseases is a decrease in TLC

45
Q

Pathophysiology of Pulmonary Edema

what can be the cause?

Cardiogenic Edema characteristics?

A

Pulmonary edema is due to leakage of intravascular fluid into the interstitium of the lungs and eventually into the alveoli. Acute pulmonary edema can be caused by increased capillary pressure (hydrostatic or cardiogenic pulmonary edema) or by increased capillary permeability.

  • Cardiogenic pulmonary edema is characterized by marked dyspnea, tachypnea, and signs of sympathetic nervous system activation (hypertension, tachycardia, diaphoresis) that is often more pronounced than that seen in patients with increased permeability pulmonary edema.
  • Pulmonary edema caused by increased capillary permeability is characterized by a high concentration of protein and secretory products in the edema fluid. Diffuse alveolar damage is typically present with the increased permeability pulmonary edema associated with acute respiratory distress syndrome (ARDS).
46
Q

Samples of Non- cardiogenic Pulmonary Edema

A
  • Aspiration
  • Neurogenic problems
    • CNS injury - vasoconstriction – blood to pulm circulation – increased pulmonary capillary pressure
  • Opiods overdose
  • High - altidue pulmonary edema
  • Re-expansion of collapsed lung
  • Negative pressure pulmonary edema
47
Q

Management of Anesthesia for Pulmonary Edema

Pre-Op

Intra-Op

Post-Op

A

Pre-op: elective surgery should be delayed

Intra-op

  • Careful wil vent settings: consider lower TVs and higher RR
  • Evaluate ABGs and/ or clinical picture
  • Extubation after careful consideration

Post -Op

  • Vented to ICU or not
  • CXR
48
Q

What is Atelectasis?

A

** recruitment breaths after intubation

49
Q

Pathophysiology of Chronic Intrinsic Lung Disease

A

Pulmonary Fibrosis Interstitial lung disease is characterized by changes in the intrinsic properties of the lungs and is most oten caused by pulmonary fibrosis. This produces a chronic restrictive form of lung disease. Pulmonary hypertension and cor pulmonale develop as progressive pulmonary fibrosis results in the loss of pulmonary vasculature. Dyspnea is prominent, and breathing is rapid and shallow.

50
Q

Management of Anesthesia in Patients With
Chronic Interstitial Lung Disease

A
  • Often has dyspnea and non-productive cough
  • Hypoxemia with normocarbia
  • Apneic periods poorly tolerated [small FRC low O2 stores]
  • POSITIONING: GA supine position and controlled ventilation further decreases FRC
  • Uptake of VA is faster because of decreased FRC
  • Lower PIP to prevent barotrauma
51
Q

What are the causes of Restrictive vs Extrinsic Restrictive

A
  • Acute intrinsic restrictive lung disease
    • ARDs, Aspiration, Neurogenic problems
  • Chronic Intrinsic Restrictive lung disease (Interstitial)
    • Sarcoidosis
    • Lymphangioleiomyomatosis
    • Hypersensitivity pneumonitis
    • Alveolar proteinosis
  • Chronic extrinsic restrictive lung disease (chest wall , pleura, or mediastinum)
    • Scoliosis
    • Pneumothorax
    • Mediastinal mass
52
Q

Pathophysiology of Sarcoidosis

what is the most common neurologic involvement

A
  • Systemic granulomatosis
  • Can affect almost any organ system in the body
    • 90 % of cases affect the the lungs; up to 50% dyspnea and cough
  • Unilateral facial palsy –> most common neurologic involvement.
  • Endobronchial sarcoid is common; larygeal sacrcoidosis (5%)
  • Hypercalcemia - classic manifestation (10%)
  • More than 50% of cases resolve without treatment
  • Tx: Glucocorticoids
53
Q

Pathophysiology: Lymphangioleiomyomatosis

A
54
Q

Intraoperative Managament of Intrinsic Restrictive Lung Disease

A
  • Apnea is very poorly tolerated
  • GA, supine position, trendelenberg position, and controlled ventilation further decrease FRC
  • Smaller ETTs may be indicated
  • What about uptake of inhaled anesthetics?
  • Watch peak airway pressures – consider pressure ventilation
55
Q

Chronic Extrinsic Restrictive Lung Disease

etiologies, association, pathology

A
56
Q

Pathophysiology: Neuromuscular Disorders

<em>(In contrast to mechanical disorders of the thoracic cage, in which an efective cough is typically preserved, the expiratory muscle weakness characteristic of neuromuscular disorders prevents generation of a sufficient expiratory airlow velocity to provide a forceful cough.)</em>

A
57
Q

Management of Anesthesia: Chronic Extrinsic Restrictive Lung Disease

A
  • If surgery is necessary , optimize the patient pre-operatively
  • Elective surgery should be postponed in acute/severe conditions
  • Restrictive lung disease contribute to the risk of post-operative complications
  • If mediastinal mass –> CT should be perfomed pre-anesthetic
    • Potential difficult airway
    • Avoid long acting -resp depressants
58
Q

Pre-Anesthetic Evaluation: Chronic Extrinsic Restrictive Lung Disease

A
  • Surgical/ Anesthesia History
  • Medical History
  • Previous intubation? Difficulty? how was it done?
  • Consultation(s) necessary/appropriate?
  • Respiratory focused assessment:
    • SOB?
    • SOB w/ exertion?
    • Fatigue?
    • Daytime sleepiness?
    • O2 at home?
59
Q

Pre-Anesthetic Evaluation (cont)

for Chronic Restrictive Lung Disease

A
  • Smoking history
  • Recent URIs
  • Medications
  • Snoring at night
  • OSA
  • STOP- BANG
  • Type of work?
  • Exercise tolerance
  • Airway assessment
  • Lung Assessment
  • Heart Assessment
60
Q

Recommendations to Reduce Perioperative Pulmonary Complications

Who are the patient’s at risk?

A
  • >60 years old
  • ASA physical class II or greater
  • Functionally dependent
61
Q

Recommendations to Reduce Perioperative Pulmonary Complications

What are the procedures that increase risk?

A
  • GA
  • Procedures >2.5 hours
  • Emergency Surgery
  • Type of Surgery
62
Q

Pathophysiology: Acute Respiratory Failure

How is ARDS Diagnosed?

<em>What are Clinical Disorders Associated With Acute Respiratory Distress Syndrome?</em>

A

Adult ARDS is caused by inlammatory injury to the lung and is manifested clinically as acute hypoxemic respiratory failure.

ARDS is now classified as<strong> mild (200 mm Hg < Pao2/Fio2 ≤ 300 mm Hg), moderate (100 mm Hg < Pao2/ Fio2 ≤ 200 mm Hg)</strong> or severe<strong> (Pao2/Fio2 ≤ 100 mm Hg)</strong>. The calculation of the Pao2/Fio2 ratio must now be calculated with CPAP or PEEP of at least 5 cm H2O.

63
Q

Where is the hypoxia from in regards to ARDS?

A
  • Alveolar damage, capillary damage, edema, inflammatory processes, V/Q mismatch, atelectasis, decrease thoracic compliance, increased dead space, hypoxic vasoconstrictions
64
Q

What are the phases of ARDS and the symptomatology

A
  1. Exudative (Frist 7 days) : High permeability , pulmonary edema
  2. Proliferative (8-21 days): interstitial inflammation
  3. Fibrotic (After 3-4 weeks): Fibrosis
65
Q

What is the Berlin Definition of ARDS

A

different levels of ARDS

28% patients 45% mortality

66
Q

Treatment Goals for ARDS

A
  1. Correct hypoxemia
  2. Removal of excess CO2
  3. Securing a patent upper airway
  • Search for underlying cause and treat it
  • Provide adequate nutrition, prevent GI bleeding and thromboembolism
  • Systemic inflammatory response syndrome (SIRS) and MODS can result
67
Q

single most predictor of nosocomial pneumonia..

Management of ARDS

A

intubation

Management of ARDS

  • Infections
  • Alveolar overdistention
  • Lung- protective ventialtion
  • Manage atelectasis
  • Polyneuropathy of critical illness
68
Q

Treatment of ARDS

(Boyd)

A
  • Pressure control ventilation
  • Pulmonary Toilet
  • TV 6-8 ml/kg
  • PEEP
  • Recruitment maneurvers
  • Maintain UO >0.5 ml/kg/hr
  • Diuretics
  • Inotropic support
  • Control infection
  • Inhaled Beta-adrenergic agonist
  • Glucocorticoid
  • Nutritional support
69
Q

What are the s/s of Pulmonary Thromboembolism

what are the tell tale sign

A

Acute dyspnea

Tachypnea

Pleuritic chest pain

70
Q

What would your capnography tell you when your patient is having PE?

If you are in Sx and you suddenly see these signs it may indicate PE

A

Sharp and sudden decrease in ETCO2

represents deadspace ventilation

  • Unexplained arterial hypoxemia, hypotension, tachycardia, or bronchospasm
  • Pulmonary HTN
  • RV dysfunction
  • Capnography - sharp and sudden deacrease
  • Spiral CT is diagnostic
71
Q

Treatment of Acute PE

A
  • Symptom driven management
  • Anticoagulation
  • Vena cava filter
  • Thrombolytic therapy
  • Hemodynamic support
  • Analgesia
  • Surgical Embolectomy

**thoracotamy, bypass

72
Q

When can you expect a fat embolism? (time frame)

what are the s/s?

What is the treatment?

A

Typically 12- 72 hours post long bone fx

Symptoms

  • Hypoxia
  • Mental confusion, sz, coma
  • Petechiae (over necj, shoulders, chest)

Treatment

  • Management of ARDS
  • Immobilization of long bone fracture
  • Corticosteroids
73
Q

O2 transport and blood oxygen content

A
74
Q

Dissolved O2 calculation

How much O2 is dissolved in blood?

A
75
Q

How to calculate the amount of CO2 in the blood

A
76
Q

O2 exchange and arterial oxygenation

A
77
Q

Estimation of PaO2 Based on Age

A
78
Q

Caculatinf A-a Gradients

A
79
Q

Elimination of CO2

How is it represented?

What qualifies as hypercarbia

S/S of Acute Hypercarbia

A
80
Q

West Lung Zones

what happens when the patient is lying down?

A

Zone 1 : Ventilating not perfusing

Zone 2: Perfusing and ventilating (Arterial pressure greater than alveolar pressure. greater than venous presseure)

Zone 3: Not ventilating only perfusinf

81
Q

What happens in the zones of the lungs if the patient changes in position from upright to supine?

A
82
Q

What happens in the zones of the lungs when the patient becomes hypovolemic?

A
83
Q

What happens if a patient suffers a C5- C6 spinal cord injury

A

patient is still spontaneously breathing but injury to C5 -C6 will affect acessory muscles

84
Q
A

Coexisting (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions