Ventilation & Gas Exchange (Ch. 31)-- Definition First Flashcards

Exam 2

1
Q

Movement of blood through pulmonary circulation

A

Perfusion

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2
Q

O2 from air in alveoli diffuses into blood in pulmonary capillaries

CO2 moves from blood in pulmonary capillaries into alveoli

Location– Alveolar-capillary membrane

A

Gas Exchange

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3
Q
  • Traumatic
  • Tension
  • Spontaneous
A

Types of Pneumothorax

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4
Q

Newborns

  • Lack of surfactant
  • Aspiration of amniotic fluids
A

Primary Atelectasis

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5
Q

Adults

  • Airway obstruction
  • Lung compression– tumor, exudate, pneumothorax

risk factors– sedation, pain, narcotics, immobility

A

Acquired Atelectasis

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6
Q

Sudden inflammation that starts at the lungs → Disruption of gas exchange at alveolar-capillary membrane

  • Hypoxemia
    • Less severe form
A

Acute Lung Injury (ALI)

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7
Q
  • S/S Primary Chronic Lung Disease– Chronic Bronchitis
    • Cyanosis
    • Polycythemia
      • ⇡ RBCs
    • ⇣ SpO2
    • Drowsiness
    • Altered Mental Status (AMS)
      • ⇡ CO2
  • S/S R Sided HF
    • Venous congestion
    • Peripheral edema
    • SOB
    • Productive cough

Management– Treatment of lung disease & HF, Low-flow O2 Therapy

A

Cor Pulmonale Manifestations

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8
Q

Collection of fluid in the pleural cavity

A

Pleural Effusion

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9
Q

Hypoxemia, ⇡ RR, absent breath sounds, dyspnea, chest asymmetry

Treatment– Fix cause, supplement O2, thoracentesis (large needle aspiration)

Tension– ⇡ HR, ⇣ cardiac output, shock, tracheal deviation (treat w/ chest tube)

A

Pneumothorax Clinical Manifestations

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10
Q

Limited expiratory airflow →Trapped air → Flattened diaphragm

Low V/Q–

  • Bronchial Asthma
  • COPD
  • Cystic Fibrosis (CF)
A

Obstructive Airway Disorders

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11
Q

⇡ Pulmonary artery pressure with normal LV pressure

d/t– Genetics, Venous HTN, Hypoxemia, Thrombotic/Embolic Disease, Pulmonary Fibrosis

  • SOB
  • ⇣ Exercise tolerance
  • R HF
  • Peripheral edema
    • Legs/ankles
  • Functional limitations
    • ⇣ ability to perform ADLs

⇡ Pulmonary artery pressure AND HF or Lung Disease

d/t– COPD, HF, Sleep Apnea, PE, Interstitial Lung Disease

  • Chronic Hypoxemia
    • Pulmonary blood vessels constrict
  • Resistance to pulmonary venous drainage
    • Diastolic dysfunction of LV
    • Mitral/Aortic valve disorders
    • Chronic thromboembolism
A

Pulmonary Hypertension Clinical Manifestations

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12
Q

PaO2 < 60 mmHG d/t problem with O2 uptake

Causes– COPD, severe PNA, Atelectasis, ARDS, Pulmonary edema, V/Q mismatch (d/t shunt, dead air space…)

  • Decreased O2 to alveoli (d/t high altitude or hypoventilation)
  • Impaired diffusion of O2 from alveoli to blood (d/t V/Q mismatch or alveolar-capillary impairment)
    • Vasodilation (Systemic circulation)
  • Inadequate circulation through pulmonary capillaries (d/t pulmonary embolus or arteriovenous malformation)
    • Pulmonary blood vessels constrict
A

Hypoxemic/Oxygenation Failure

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13
Q

Loss of negative pressure in pleural cavity → Collapsed lung

  • Pleural effusion
  • Pneumothorax
  • Atelectasis
A

Disorders of Lung Inflation

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14
Q

Chest Injury (penetrating or non-penetrating)

  • fractured or dislocated ribs
  • CPR
  • Central line insertion
  • Intubation
  • Positive pressure ventilation
A

Traumatic Pneumothorax

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15
Q

Oxygenated Blood

A

Pulmonary Veins

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16
Q

Movement of O2 and CO2 across the alveolar-capillary membrane

A

Diffusion

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17
Q

Clear, thin fluid (hydrothorax), specific gravity <1.020

d/t– CHF, renal failure, nephrosis, liver failure, malignancies (cancer)

A

Transudate

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18
Q

Infection in pleural cavity d/t exudate

A

Empyema

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19
Q

High V, Low Q (100:1)

  • Dead air space
  • Low flow states
  • Pulmonary embolism (PE)
A

High V/Q

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20
Q

Exaggerated Type I IgE-mediated hypersensitivity response to inflammatory mediators

Leads to–

  • Bronchoconstriction
  • Vascular permeability
  • ⇡ Mucus production
  • Prolonged expiration → Air trapping
    • Lung hyperinflation
    • ⇡ Pulmonary artery pressure
A

Atopic Asthma Etiology

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21
Q

Reduced oxygenation of cells in tissues

  • Does not always indicate reduced oxygenation of arterial blood
A

Hypoxia

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22
Q
  • Cyanosis
  • Fluid retention
    • R-sided HF (cor pulmonale)
  • Productive cough
  • ⇣ RR
  • Crackles and wheezes
    • d/t mucus in the lungs
A

Chronic Bronchitis Clinical Manifestations

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23
Q

Abnormal elevation of pressure within pulmonary arterial circulation

  • ⇣ Size of lumen in pulmonary arteries
    • Vasoconstriction → Hypoxia
  • ⇡ Inflow of blood to pulmonary arteries
  • Occlusion of outflow of blood from pulmonary circulation
    • ⇡ Pressure in LV
A

Pulmonary Hypertension

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24
Q

⇣ Lung elasticity & abnormal enlargement of air spaces → Alveolar wall & capillary bed destruction

  • ⇡ Serine elastase (Protease) release from neutrophils → Digestion of elastic fibers → ⇣ Alveolar recoil
  • Lung hyperinflation → ⇡ Total lung capacity

d/t– Genetics, Smoking, Alpha 1 antitrypsin (AAT) (antiprotease enzyme) deficiency

A

Emphysema Etiology

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25
Q

Pulmonary insult → Inflammatory response (neutrophils secrete proteases, cytokines, & ROS)

Permeability of alveolar-capillary membrane → Fluid, plasma, proteins, and blood cells into interstitium & alveoli

Loss of surfactant & damage (Type I & Type II pneumocytes) → ⇣ Pulmonary compliance → Lung collapse

Injury to alveolar epithelium → Disorganized repair → Fibrosis → Lungs stiffen (difficult to inflate, ⇡ WOB)

⇣ Gas exchange at alveolar-capillary membrane → ⇡ Intrapulmonary shunting (find alveolus that has O2) → ⇣ V/Q Ratio

Hypoxemia refractory to supplemental O2 → Alveoli collapse

A

ALI/ARDS Pathophysiology

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26
Q

⇡ RR, ⇡ HR, dyspnea, cyanosis, hypoxemia, decreased chest expansion, absent breath sounds, intercostal retractions

Prevention– incentive spirometer, frequent position changes, ambulate, hydrate

Treatment– fix cause, supplemental O2

A

Atelectasis Clinical Manifestations

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27
Q

Sudden inflammation that starts at the lungs → Disruption of gas exchange at alveolar-capillary membrane

  • Life-threatening Hypoxemia
    • Refractory to supplemental O2 Therapy
  • Diffuse crackles
  • Dyspnea
    • Severe, sudden onset
    • w/i 12-18 hrs. of insult
  • Hypoxia
  • Cyanosis
  • Tachypnea
    • ⇡ RR
  • Tachycardia
  • Diaphoresis
    • Sweating
  • Pulmonary infiltrates
    • White on x-ray
  • Systemic response
    • Multiple organ failure dysfunction syndrome (MODS)
      • Renal, GI, CV, CNS
A

Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations

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28
Q

Thick mucus hypersecretion → Mucus plugs → Gas trapped in distal portion of lungs

  • Lung hyperinflation
  • Chronic, productive cough
  • Smoking
    • ⇡ mucus production
    • ⇡ size and # of mucus glands
A

Chronic Bronchitis Etiology

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29
Q

Prevention is key

  • DVT Prevention
    • Hospital
      • Sequential Compression Devices (SCDs)
      • Heparin (SC)
        • 2X/day
    • Outpatient
      • Warfarin (PO)
      • Lovenox (SC)
        • Low molecular wt. heparin
  • Multiple or large pulmonary emboli
    • Thrombolytic therapy
      • Streptokinase
      • Anistreplace
      • Recombinant tissue plasminogen activators (tPA)
        • “clot buster”
          • MI/Stroke
A

Pulmonary Embolism Treatment

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30
Q

Reduced oxygenation of arterial blood

  • Always leads to reduced oxygenation of cells in tissues
A

Hypoxemia

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31
Q

Space between parietal pleura and visceral pleura

A

Pleural Cavity

32
Q

Air stuck in pleural space (intrapleural pressure > atmospheric pressure)

Leads to–

  • compression atelectasis
  • trachea and sternum shift L
  • L lung shift
  • Vena cava compression
  • ⇣ venous return
  • ⇣ cardiac output
A

Tension Pneumothorax

33
Q
  • Accessory muscle & pursed-lip breathing
    • ⇡ positive pressure
  • Barrel chest
    • d/t air trapping
  • ⇣ Breath sounds
  • ⇡ RR
  • Non-productive cough
  • NO cyanosis
A

Emphysema Clinical Manifestations

34
Q

Low V, High Q (1:100)

  • Shunt
  • Chronic bronchitis
  • Asthma
A

Low V/Q

35
Q

Brain, lungs, and heart need O2 Compensatory mechanisms activate

⇣ O2 → Anaerobic Metabolism → ⇡ Lactic Acid → Metabolic Acidosis

A

Hypoxemia Etiology

36
Q
  • Cl- unable to move into epithelial lumen of airway
    • Cl- remains w/i cell
    • Na+ & H2O move from airway into blood
      • Respiratory secretions thicken
  • H2O in mucous membranes
    • Dehydration
    • Accumulation of mucus
      • Airway obstruction
      • Pancreatic & biliary duct dysfunction
        • Pancreatic enzyme deficiency
      • Vas deferens dysfunction
        • Azoospermia
  • Increased risk of pulmonary infection
A

Cystic Fibrosis Pathogenesis

37
Q
  • Small emboli
    • Asymptomatic
      • Not usually
  • Moderately-sized emboli
    • Rapid, shallow respirations
    • Pleuritic pain
    • Cough
      • Blood-streaked sputum
  • Massive emboli
    • Sudden collapse
    • Crushing substernal chest pain
      • Can be confused w/ MI
    • Shock
    • LOC
    • Rapid, weak pulse
    • Hypotension
    • Distended neck veins (JVD)
    • Cyanosis
    • Fatal
A

Pulmonary Embolism Clinical Manifestations

38
Q

Movement of air into the lungs

A

Ventilation

39
Q

Deoxygenated Blood

A

Pulmonary Artery

40
Q

Chronic and recurrent obstruction of expiratory airflow

  • Chronic Bronchitis
  • Chronic Emphysema
A

COPD Types

41
Q

Limit exposure to allergens

Pharmacologic Agents

Immediate

  • Bronchodilator
    • Albuterol (SABA)
  • Anti-Inflammatory
    • Corticosteroid (ICS)

Long-Term

  • Mometasone (ICS)
  • Salmeterol (LABA)
  • Symbicort– Combination (LABA + ICS)
A

Asthma Treatment

42
Q

Extrinsic/Allergic/Atopic Response

  • 2-8 hrs. after exposure
  • Mucosal edema, ⇡ secretion, ⇡ WBC, epithelial damage, bronchospasm
  • Lasts several days

Treatment– Corticosteroids (ICS)

A

Late Phase Response

43
Q

Goals–

  • Oxygenate lungs and vital organs
  • Recognize & treat underlying medical condition
  • Prevent further injury and complications
    • Venous thromboembolism
    • Aspiration
    • Infection
  • Decrease risk for mortality

Treatment– Intubation & Mechanical ventilation

A

ARDS Treatment

44
Q

Beta-adrenergic receptors → Bronchodilation

A

Sympathetic Stimulation

45
Q

CO2 in the arterial blood → Hypercapnia/Hypercarbia → Respiratory Acidosis

d/t– ⇣ RR

A

Hypoventilation

46
Q

⇣ CO2 in the arterial blood → Hypocapnia/Hypocarbia → Respiratory Alkalosis

d/t– Panic attack, pain, ⇡ RR, hypoxemia

A

Hyperventilation

47
Q

Air in pleural space → ⇡ Pressure → Partial or complete lung collapse

A

Pneumothorax

48
Q
  • Inadequate gas exchange
  • V/Q mismatch
  • PaO2 < 60 mmHg or PaCO2 > 50 mmHg & pH <7.30 or BOTH
    • Severe Hypoxemia + Hypercapnia + Respiratory Acidosis
  • Post-Surgery
    • Atelectasis
    • PNA
    • Pulmonary edema
    • Pulmonary emboli → Respiratory failure
  • Smoking + lung Disease
  • Underlying disease/infection
    • Renal, cardiac, neurologic, or hepatic
A

Respiratory Failure Manifestations

49
Q
  • Respiratory
    • Accumulation of thick mucus in bronchi
    • Impaired mucociliary clearance
    • Lung infections
      • Bronchiectasis
        • Mucus buildup in the lungs
    • Chronic bronchitis/bronchiolitis
  • Abnormal pancreatic function
    • Steatorrhea
      • Fatty stool
    • Diarrhea
    • Abdominal pain
    • Malabsorption
    • Malnutrition
A

Cystic Fibrosis Clinical Manifestations

50
Q

Perfusion without ventilation (LOW V/Q)

  • Hypoxemia
  • Atelectasis
  • PNA
  • Asthma
  • COPD
    • Chronic bronchitis
    • Emphysema
A

Shunt

51
Q

Histamine, leukotrienes, prostaglandins → Bronchoconstriction

A

Inflammatory Mediators

52
Q

Incomplete expansion of lung/alveoli

d/t– Pleural effusion, Pneumothorax, loss of surfactant

A

Atelectasis

53
Q

PaCO2 > 50 mmHg AND pH <7.30

Causes– ⇣ RR or WOB

  • Upper airway obstruction– infection, laryngospasm, tumors
  • Weakness or paralysis of respiratory muscles– brain injury, sedation, drug overdose (opioids), Guillen-Barre syndrome, Muscular Dystrophy, spinal cord injury
  • Chest wall injury– physiologic dead space

Leads to– Vasodilation (systemic circulation), Pulmonary blood vessel constriction

Diagnosis

  • ABG– elevated CO2
A

Hypercapnic/Ventilation Failure

54
Q

Low V, Very High Q (1:1000)

  • Atelectasis
  • ARDS
  • Pneumonia
A

Very Low V/Q

55
Q
  • Genetic
    • Autosomal recessive
  • Chronic respiratory disease
    • Exocrine glands in epithelium of respiratory, GI, & reproductive tracts
      • Pancreatic exocrine deficiency
      • ⇡ NaCl in sweat
    • Mutation in cystic fibrosis transmembrane regulator (CFTR)
      • Chloride channel in airway epithelium
        • Impermeable to chloride
A

Cystic Fibrosis

56
Q

Dyspnea, Hypoxemia

  • ⇣ lung expansion on affected side
  • Dull to percussion
  • ⇣ breath sounds

Treatment– antibiotics, thoracentesis (large needle aspiration), chest tube

A

Pleural Effusion Clinical Manifestations

57
Q

Purulent, thick fluid, specific gravity >1.020

d/t– elevated LDH & protein, inflammatory cells

A

Exudate

58
Q

Acute:

Mild– SANS activation

  • ⇡ HR,
  • ⇡ RR
  • ⇣ mental acuity
  • Vasoconstriction
  • Pale skin
  • Diaphoresis

Moderate/Severe– Altered mental status

  • Confusion
  • Stupor
  • Coma

Chronic:

  • ⇡ RR
  • Pulmonary vasoconstriction
  • Polycythemia (⇡ RBC)
  • Cyanosis
  • Clubbing
A

Hypoxemia Clinical Manifestations

59
Q
  • Aspiration
    • Near drowning
    • Gastric contents
  • Drugs & Toxins
    • Heroin
    • Free-base cocaine smoking
    • Inhaled gases
      • Smoke, ammonia
    • High O2 Concentrations
    • Radiation
  • Infections
    • Sepsis
  • Trauma & Shock
    • Burns
    • Fat embolism
    • Chest trauma
  • Disseminated Intravascular Coagulation (DIC)
    • Multiple blood transfusions
A

ALI/ARDS Causes

60
Q

Ventilation without perfusion (HIGH V/Q)

  • Hypoxemia
A

Dead Air Space

61
Q
  • Smoking cessation
  • Avoid bronchospasm triggers
  • Pulmonary rehab
    • ⇡ efficiency
    • ⇣ WOB
  • Prevent RTIs
  • Bronchodilators
    • Albuterol (SABA)
  • Anticholinergics
    • Ipratropium bromide
  • O2 therapy w/ significant hypoxemia (PaO2 < 55 mmHg)
    • 1-2 L low-flow oxygen
      • Limit to stimulate breathing
      • Goal: PaO2 55-65 mmHg
      • Goal: SpO2 88-92%
A

COPD Treatment

62
Q

Chronic inflammation of airway → airflow obstruction & airway hyperresponsiveness

  • Extrinsic/Allergic/Atopic
    • Type I IgE-mediated hypersensitivity reaction
    • Genetic component
  • Intrinsic/Non-allergic/Non-Atopic
    • no allergy component
A

Bronchial Asthma Types

63
Q
  • Airways narrow d/t
    • Bronchospasm
    • Bronchial mucosal edema
    • Mucus plugging
  • Prolonged expiration → Air trapping
    • Lung hyperinflation
  • ⇡ WOB → ⇡ O2 demands
    • Dyspnea
    • Fatigue
  • ⇣ Alveolar ventilation → Low V/Q
    • Hypoxemia
    • Hypercapnia
A

Asthma Clinical Manifestations

64
Q

Pulse Oximetry

Arterial Blood Gas (ABG)

A

Measures of blood oxygenation

65
Q

Diagnosis–

  • Respiratory & GI manifestations
  • Family history
  • Newborn screening
    • + = ⇡ immunoreactive trypsinogen
  • Sweat chloride test
    • 2X normal NaCl in sweat
  • CFTR functional testing & genetic analysis

Treatment–

  • Goal: Slow progression of secondary organ dysfunction
    • Chronic lung infection
      • Antibiotics
      • Bronchodilators
      • Chest percussion
      • Postural draining
    • Pancreatic insufficiency
      • Pancreatic enzyme replacement
      • Vitamin supplements
A

Cystic Fibrosis Diagnosis & Treatment

66
Q
  • RTIs
  • Exercise (EIB)
  • Drugs
    • ASA– ⇣ COX, ⇡ LOX → ⇡ Leukotrienes
    • Morphine– Histamine release
  • Emotional Upset
  • Bronchial irritants
    • Smoke
    • Toxins
A

Asthma Attack Triggers

67
Q

Virchow Triad

  • Venous stasis (slowing) & Venous endothelial injury
    • Bed rest, hip or femur fracture, surgery, childbirth, MI, HF, spinal cord injury
  • Hypercoagulability states
    • Cancer
    • Pregnancy
    • HRT
    • Oral contraceptives
A

Pulmonary Embolism Risk Factors

68
Q
  • Hypoxemic– Oxygenation Failure
  • (PaO2 < 60 mmHg)
    • COPD
    • PNA
    • Atelectasis
    • Impaired diffusion
      • Pulmonary edema
      • ALI/ARDS
  • Hypercapnic/Hypoxemic– Ventilation & Oxygenation Failure
  • (PaO2 < 60 mmHg, PaCO2 > 50 mmHg & pH <7.30)
    • Upper airway obstruction
      • Infection
      • Laryngospams
    • Weakness or paralysis of respiratory muscles
      • Brain injury
      • Overdose
      • Guillain-Barre
      • Muscular Dystrophy
      • Spinal Cord Injury
    • Chest wall injury

Diagnosis– ABGs (determine if hypoxemic, hypercapnia or BOTH)

A

Types of Respiratory Failure

69
Q

VQ ratio not 1:1

  • Ventilation (V)
  • Perfusion/Blood Flow (Q)
A

VQ Mismatch/Inadequate Gas Exchange

70
Q

Cholinergic receptors → Bronchoconstriction

A

Parasympathetic Stimulation

71
Q

Bloodborne substances lodged in pulmonary artery → Bloodflow obstructed (High V/Q)

d/t– Thrombus (DVT) → Pulmonary circulation, Injected air (IV), Fat mobilization after long bone fracture (femur, humerus, pelvis), Amniotic fluid entering maternal circulation during childbirth

A

Pulmonary Embolism

72
Q

Blood in pleural cavity d/t lung puncture (trauma)

  • Chest injury, chest surgery complications, malignancies, rupture of great vessel (aortic aneurysm)

Treatment– Chest tube

A

Hemothorax

73
Q

Right Sided Heart Failure

d/t– Primary Lung Disease, Pulmonary Hypertension, Chronic Bronchitis

  • ⇡ Pulmonary circulation pressures
    • Fluid retention
      • ⇡ Work of RV
      • Hypertrophy → R sided HF
A

Cor Pulmonale

74
Q

Bleb/Blister ruptures → Air flows from alveoli into pleural space

Primary

  • Bleb @ top of lungs
    • Tall, thin people
    • Smokers

Secondary

  • Lung disease
    • Asthma, TB, CF, COPD, lung CA
    • Potentially life threatening
A

Spontaneous Pneumothorax

75
Q

Extrinsic/Allergic/Atopic Response

  • 5-30 mins. after exposure
  • ⇡ Release of inflammatory mediators
  • Vasodilation, vascular damage, bronchospasm

Treatment– Albuterol (SABA)

A

Early Phase Response