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NURS 2360 Med/Surg > Exam 2 Respiratory > Flashcards

Exam 2 Respiratory Flashcards

1
Q

What is a VQ mismatch?

A

A ventillation and perfusion mismatch

Either part of the lung receives oxygen with no blood flow, or blood flow with no oxygen

Occurs when there is an obstruction either in the airway (choking) or blood vessel (Clot)

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2
Q

What causes a VQ mismatch that effects perfusion?

A

pulmonary embolism

pulmonary hypertension

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3
Q

What causes a VQ mismatch that effects ventillation?

A

pulmonary edema

airway obstruction

asthma

COPD

cystic fibrosis

lung mass

pneumonia

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4
Q

What is the function of the alveoli?

A

site of gas exchange

surfactant keeps them open

large surface area

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5
Q

What is the difference between pulmonary artery and pulmonary vein?

A

pulmonary artery carries deoxygenated blood

pulmonary vein carries oxygenated blood

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6
Q

Pulmonary Artery

A

Most deoxygenated blood in the body

pulmonary artery pressure is lower than systemic

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7
Q

hypoxia vs hypoexmia

A

hypoxia is low O2 in the tissue

hypoxemia is low o2 in the blood

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8
Q

Respiratory diagnostic tests

A

radiology: CXR, V/Q scan, pulmonary angiography, CT scan, MRI

pulmonary function tests: PEFR, incentive spirometry

bronchoscopy: visualization, biopsy, lavage

Thorocentesis: intervention and test

ABG

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9
Q

pH normal range

A

7.35 - 7.45

> 7.45 = alkalotic

<7.35 = acidic

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10
Q

CO2 normal range

A

35-45 (acid)

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11
Q

HCO3 normal range

A

22-28 (base)

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12
Q

Alkalosis

A

pH > 7.45

too much base (HCO3)

too little acid (CO2)

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13
Q

Acidosis

A

pH < 7.35

too much acid

too little base

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14
Q

What happens if the respirations are too low?

A

carbon dioxide can’t leave the plasma and CO2 builds up

there will be an INCREASE in CO2 = more acidic blood = pH decreases

respiratory acidosis

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15
Q

What causes respiratory acidosis?

A

asthma, COPD, pneumonia

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16
Q

What happens if respirations are too high?

A

carbon dioxide leaves the plasma and is exhaled

there will be a DECREASE in CO2 = less acid in blood = pH increases

respiratory alkalosis

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17
Q

What causes respiratory alkalosis?

A

anxiety, pulmonary embolism, fever

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18
Q

What happens if there is a metabolic problem?

A

The body is creating too much acid or base, so the lungs will try and compensate by reataining or blowing off CO2

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19
Q

metabolic acidosis causes

A

shock, lactic acidosis, DKA, diarrhea

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20
Q

metabolic alkalosis causes

A

vomiting, diuretic use

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21
Q

uncompensated ABG

A

opposite system has not attempted to compensate and remains normal

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22
Q

partially compensated ABG

A

opposite system is outside normal range to try and compensate, but pH is still abnormal

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23
Q

compensated ABG

A

opposite system is outside normal range in an effort to compensate, pH is normal

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24
Q

how to tell if a problem is respiratory or metabolic?

A

ROME

respiratory opposite - arrows go opposite directions for pH and CO2

metabolic equal - arrows go the same direction for pH and HCO3

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25
Q

hypoxemic patient

A

paO2 low (<60) while receiving FiO2 of 60%

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26
Q

hypercapnic patient

A

paCO2 >45 with acidemia (pH <7.35)

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27
Q

acute respiratory failure

A

patient will either be hypoxemic or hypercapnic or mixed

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28
Q

Acute Respiratory Failure S&S

A

tachypnea

deep respirations (acidosis)

use of accessory muscles

dysrhythmias

confusion/restless

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29
Q

Acute respiratory failure collaborative care

A

treat underlying cause and reverse the 3 areas of compromise

  1. treat underlying pulmonary problem
  2. treat anxiety and restlessness
  3. oxygenation
  4. correct acidosis
  5. mobilization of secretions
  6. nutritional therapy
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30
Q

How to treat underlying pulmonary congestion?

A

diuretics

vasodilators

antihypertensives

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31
Q

How to treat pulmonary infection?

A

antibiotics

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32
Q

How to treat pulmonary inflammation

A

corticosteroids

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33
Q

How to treat bronchospasm?

A

bronchodilators, aerosol treatments

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34
Q

how to treat anxiety and restlessness?

A

correct CO2/O2 problem

low dose anxiety medication

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35
Q

How to correct acidosis?

A

hyperventilate

bicarb drip

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36
Q

acute respiratory failure nutritional therapy

A

high caloric and high protein

caution!* NG feedings while on CPAP/BIPAP

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37
Q

high flow nasal cannula

A

7-15 L/min

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38
Q

airvo

A

up to 100% fio2 at 60L/min

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39
Q

CPAP vs BiPAP

A

CPAP decreases work of breathing on inspiration

BIPAP is pressure on inspiration and expiration - better for COPD. Can help repell trapped CO2

40
Q

Criteria for CPAP and BIPAP

A
  1. patient must be able to protect their airway (gag/cough intact, patent, can swallow, low aspiration risk, low secretions)
  2. Will the disease process likely to improve within the next 48-72 hours?
41
Q

What type of patient will benefit from CPAP/BIPAP?

A

acute respiratory failure (hypercapnia)

COPD

cardiogenic pulmonary edema

option for DNI patietns

42
Q

advantages of CPAP/BIPAP

A

non-invasive

decreased r/o pneumonia

no tracheal damage

no sedation

can be easilly removed and reapplied

can be used in non ICU setting

43
Q

mechanical ventilation

A

improve tissue O2 that cannot be maintained by other forms of O2 therapy

requires intubation

44
Q

tracheostomy complications

A

tracheal wall necrosis

tracheal dilation

tracheal stenosis

fistula formation

airway obstruction

infection

accidental decannulation

subcutaneous emphysema

45
Q

What is PEEP

A

positive end expiratory pressure - keeps airways open between breaths to reduce hypoxemia and improve V/Q ration (5-20)

46
Q

What is tidal volume

A

amount of O2 delivered with each ventillation

47
Q

What is fio2

A

% of o2 delivered with each breath

48
Q

Mechanical Ventilation Complications

A

ventillator assisted pneumonia

barotrauma

pneumothorax

GI effects

Cardiac effects

49
Q

Causes of pulmonary edema

A
  1. Cardiogenic pulmonary edema
    - heart problems (valve problem, CAD, left ventricular dysfunction/failure, fluid overload)
  2. Impaired endothelium (lining of capillary)
  3. lymphatic obstruction
50
Q

Cardiogenic pulmonary edema

A

blood backflows into pulmonary vasculature > increased hydrostatic pressure > EDEMA > acute respiratory failure

causes: valve problem, CAD, left ventricular dysfunction/failure, fluid overload

51
Q

impaired endothelium

A

capillary endothelium - lining of the capillary

hypoalbuminemia: decreases capillary osmotic pressure

OR

injury to capillary caused by:

inhaled toxins, near drowning, inflammation

mechanical ventilation (PEEP, oxygen toxicity)

sepsis

aspiration

smoke inhalation

ARDS

52
Q

lymphatic obstruction

A

malignancies of the lymph system

lung mass compressing lymph vessels

53
Q

pulmonary edema

A

fluid in the alveoli displaces air > impaired gas exchange

decreases gas exchange! Oxygen can’t cross alveolar/capillary membrane and attach to HGB in capillary

leads to acute respiratory failure!

54
Q

pulmonary edema respiratory symptoms

A

tachypnea

labored respirations

productive cough frothy pink sputum

cough

dyspnea

crackles

paroxysmal nocturnal dyspnea

orthopnea

55
Q

pulmonary edema cardiovascular symptoms

A

tachycardia

cool, clammy skin

hypotension

hypoexmia

cyanosis

S3

56
Q

pulmonary embolism neurological symptoms

A

restlessness

feeling of impending doom

anxiety

57
Q

classic symptoms of pulmonary edema - traid

A

dyspnea, chest pain, hemoptysis (pink/froth sputum)

58
Q

pulmonary edema diagnostic tests

A

CXR - will see white out

PA catheter (swan ganz) - fluid builds up in the PA. Increased pulmonary artery pressure - will be ELEVATED

Central venous pressure - measures preload - will be ELEVATED

SpO2

ABG

59
Q

Pulmonary edema collaorative care

A

suctioning (pulmonary toileting)

respiratory support (NC, SFM, VM, non-rebreather)

advanced respiratory support (airvo, cpap, bipap, mechanical vent)

reduce preload

reduce afterload

support perfusion

reverse cause of altered membrane permeabilty

60
Q

How to reduce preload

A

(decrease fluid in circulation)

diuretics - furosemide oral, IV push, or infusion

nitrates - nitroglycerin vasodilator IV

elevate HOB

61
Q

How to reduce afterload

A

(improves cardiac output)

calcium channel blockers: amlodipine, verapamil, diltiazem

antihypertensives

nitrates - nitroclycerin, nitroprussside

62
Q

How to support perfusion

A

increase cardiac output with + ionotropes (increase contraction): dobutamine, digoxin, dopamine

63
Q

how to reverse altered membrane permeability

A

correct hypoalbuminemia

establish fluid balance

64
Q

Pulmonary hypertension

A

increased pressure in the pulmonary artery > vascular remodeling

NO cure

can be primary or secondary

65
Q

Primary Pulmonary Hypertension

A

idiopathic

no known cause

rare

most common in women 20-40

life expectancy 2.8 years from diagnosis without treatment

66
Q

Secondary pulmonary hypertension

A

2 types: post capillary and precapillary

67
Q

post capillary pulmonary hypertension

A

distal to (after or beyond) the pulmonary capillaries- LV, LA, pulmonary veins

causes:
LV failure

mitral stenosis

occlusion of pulmonary vein

cirrhosis and portal hypertension

68
Q

Precapillary pulmonary hypertension

A

problems within the capillaries or alveoli

normally in response to hypoxia - in the lungs pulmonary vessels will CONSTRICT in response to hypoxia

causes related to hypoxia:

COPD

sleep apnea

stiffness of pulmonary vasculature (sarcoidosis)

pulmonary fibrosis

69
Q

Primary Pulmonary Hypertension Manifestations

A

syncope

dyspnea

fatigue

weakness

chest pain

hemoptysis

activity intolerance

70
Q

Secondary pulmonary hypertension symptoms

A

looks like underlying problem but more exaggerated

ex: COPD symptoms, CHF symptoms

71
Q

pulmonary HTN diagnostics

A

echocardiogram - best way
- shows tricuspid regurgitation, RV failure

CXR
- may show enlarged pulmonary artery

Right sided cardiac cath. or insertion of PA catheter
- determine PA pressure
- mean pulmonary arterial pressure will be elevated

72
Q

Pulmonary HTN complications

A

cor pulmonale ( RV dilation) leading to RV failure
- may present with systemic edema, ascites and weight gain

73
Q

Pulmonary HTN collaborative care

A

Primary: double lung transplant

Supportive: oxygen spo2 >90

74
Q

pulmonary HTN meds

A

prostanoids: vasodilators - epoprostenol sodium - continous IV or inhaltion

phosphodiesterase inhibitor/vasodilator: sildenafil

increase cardiac output: digoxin, dobutamine, dopamine

calcium channel blockers (high dose): amplodipine, diltiazem

diuretics: reduces PA pressure

Antcoagulants: warfarin, apixaban, dabigatran

75
Q

epoprostenol sodium side effects

A

jaw pain, nausea, diarrhea, infection, thromboembolism

76
Q

heparin antidote

A

protamine sulfate

77
Q

coumadin antidote

A

vitamin K

78
Q

lifestyle modifcations for pulmonary HTN

A

low sodium
fluid restriction

low intensity workout

contraception!

avoid temperature extremes

79
Q

pulmonary embolism

A

thrombus breaks loose from somewhere else and is now an embolus - once it enters pulmonary vessel it will occlude it

usually comes from legs

80
Q

pulmonary embolism origins

A

blood clot - most common

fat emboli (orthopedic surgery, broken bones)

tumor fragments

amiotic fluid

foreign body

81
Q

Severe PA occlusion

A
  • sudden death “saddle PE”
  • lung tissue infarction
82
Q

PE consequences

A

increased dead space (areas of lungs that are ventilated, but no perfused)

if infarction does not occur, firbinolytic system dissolves clot

PE - Perfusion problem that effects gas exchange

83
Q

DVT risk factors

A

(virchows triad)

  1. venous stasis
    - prolonged bed rest, obesity
  2. endothelial damage
    -vessel wall damage (phlebitis)

3 altered blood coagulation
- inhertied thrombophilia
- cancers that produce coagulation factors
- smoking
- incidence higher in African American

84
Q

PE risk factors

A

hypercoagulability:

coagulatin disorders

cancer

oral contraceptives

sepsis

following childbirth, sx, trauma

endothelial damage:

phlebitis

surgery

trauma

sepsis

85
Q

pulmonary embolism diagnosis

A
  1. D-Dimer
    - indicates high levels of fibrin products in body
  2. ABG
    - low paO2 and low PaCO2 (hyperventiliation, respiratory alkalosis)
  3. CXR
    - rule out other condition
  4. V/Q scan
    - show abnormal perfusion and normal ventilation
  5. chest CT with contrast
    - difinivie. Can visualize PE
86
Q

pulmonary embolism manifestations

A

anxiety and apprehension - impending doom

dyspnea & SOB

chest pain

tachycardia/dysrythmia

extremity swelling/pain

tachypnea and shallow respirations

cough

diaphoresis

hemioptosis

87
Q

PE prevention

A

preophylactic anticoagulants (coumadin, enoxaparin, warfarin)

SCDs

ROM/ambulation

88
Q

PE treatment

A

support and stablization cardiopulmonary system
- o2

+ionotropes (digoxin, dopamine, dobutamine) if hemodynamically unstable, inadequate output

anticoagulation therapy - haparin, warfarin, apixaban

fibrinolytic therapy if massive PE and patient is hemodynamically unstable

embolectomy

surgery (greenfield) filter

89
Q

ARDS

A

a group of symptoms: acute lung injury from unregulated systemic inflammatory response to acute injury or inflammation. Part of lung is not getting air

rapid onset of noncardiac pulmonary edema

progressive refratory hypoexemia

extensive lung tissue inflammation

multisystem organ malfunction

90
Q

ARDS mortality rate

A

smokers more common to acquire

effects men more than women

african americans more often effected

91
Q

direct causes of ards

A

effect the LUNG

pulmonary infections

aspiration of gastric contents

inhalation injuries (smoke, saltwater, drowning)

92
Q

indirected causes of ards

A

sepsis (poorer outcomes than respiratory cause)

trauma

GI infections

drug overdose

multiple blood transfusions

severe fluid overload

93
Q

stages of ards

A
  1. initiation of ards (24-48 hours before pulmonary edema) figured out after the fact
  2. onset of pulmonary edema
  3. alveolar collapse d/t surfactant deficit
  4. end-stage ards
94
Q

ards manifestations

A

intercostal retractions/use of accessory muscles

tacypnea as demand for O2 increases and patient tries to release CO2

adventitious lung sounds (Crackles), edeuma, atelactasis

CXR shows interstitial changes, patchy infiltrates

pulse ox, ABG show refractory hypoxemia

agitation, confusion, lethargy

95
Q

ards diagnostics

A

ABG to determine o2 levels

CXR or CT to assess fluid in lungs

CBC, blood chemistry, and blood culture to determine cause of ards

sputum culture

blood culture if sepsis suspected

96
Q

ARDS treatment

A

*intubation - may req. atypical ventilator and high PEEP D/T alveolar collapse and edema

*CPAP/BIPAP

*no definitive drug therapy but maybe:

vasoconstrictors (dopamine, dobutamine)

diuretics

corticosteroids

bronchodilators

NSAIDS

surfactant therapy

  • prone position

*ECMO

*insertion of PA catheter

97
Q

why is prone position good for ARDS

A

decerase dead space

reduces intrathoracic pressure and gravity forces on lung tissue (reduces atelectisis)

enhances ventillation (impoves V/Q matching)

decreases mortalitiy

NURS 2360 Med/Surg (6 decks)

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