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Pathophysiology > Patho: Respiratory > Flashcards

Patho: Respiratory Flashcards

1
Q

What are the Four processes needed for respiration?

A

1)Ventilation: Lungs expand and pressure decreases.

2)External Respiration: Gas exchange in the alveoli membrane.
Air entering the body is “air outside the body” and once it crosses the membrane then it’s considered “in”.
You need the right concentration for the concentration gradient and partial pressure for gas exchange.

3) Circulation of the gases (perfusion)
4) Internal Circulation: Gases exchange in tissue in capillaries, need proper concentration and partial pressure for proper gas exchange.

External respiration occurs in the Lungs
Internal respirtation occurs in the cells/tissues.

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2
Q

Why does Ventilation and Perfusion need to be synchronized?

A

Ventilation:
-Gas reaching the alveolo

Perfusion:
-Blood flow in the pulmonary capillaries, serves the alveoli

Must be synchronized b/c it’s more efficeint for external respiration, and to not waste blood flow.

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3
Q

What are the functions of the Respiratory System?

A

1) Providing a large area for gas exchange b/w air and circulating blood.
2) Moving air to and from has exchange surfaces of the lungs.
3) Protecting the respiratory surfaces from dehydration and temperatures changes, and defending against invading pathogens.
4) Producing sounds permitting speech, singing, and nonverbal auditory communication.
5) Aiding the sense of smell by the olfactory receptors in the nasal cavity.

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4
Q

How can Increased or Decreased PCO2 affect respiration?

A

If PCO2 increases: (Hypercapnia)
-RR increase to expel the increased PCO2

If PCO2 decreases:(Hypocapnia)
-RR decreases in order to conserve carbon dioxide (To prevent metabolic alkalosis)

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5
Q

What is PCO2?

A

Partial Pessure of Carbon dioxide.

It represents the amount of CO2 on the hemoglobin of the blood

Carbon dixoide stimulates chemoreceptors in medulla
and that stimulates inspiratory muscles to increase and helps maintain good CO2 lvls

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6
Q

What is PO2?

A

Partial Pressure of Oxygen

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7
Q

How does the Respiratory Control Work?

A

1) Increased PCO2 leads to changes in CSF(medulla) pH
2) PO2 influences chemoreceptor*(receptor that senses pH changes and respons accordingly) sensitivity to PCO2 –> PCO2 receptors incr.sensitivity
3) PO2 below 60mmHg(very low) directly stimulates breathing –>hypoxic drive

4)Decreased pH stimulates breathing
 Metoboic acidosis (Build up of lactic acid)
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8
Q

Difference b/w Peripheral and Central Chemoreceptors

A

Peripheral: Are stimulated by very low O2 levels.
-The chemoreceptors then stimulate inspiratory muscles to increase RR to expel excess CO2 and increase O2

Central: Are stimulated by high levels of CO2
-The chemoreceptors then stimulate Respiratory muscles to increase RR to expel excess CO2 and increase O2

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9
Q

What is pulmonary Edema?

A

It refers to the fluid collecting in the alveoli and intersitial space

The accumulation of fluid reduces the amount of oxygen diffusing in to the blood and interferes with:

  • lung expansion
  • reducing oxygenation of the blood

Excess fluid can develop in one of the four ways. The same ways edema develops.

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10
Q

Patho of Pulmonary Edema

A
  • Pulmonary HTN develops (Stress on the right side of the heart)
  • Normally capillary pressure is low in the lungs, as the contiain minimal fluid
  • When capillary pressure increases, this forces the fluid out of the capillaries and into the alveoli.
  • Excessive amounts of fluid interefere w/ oxygen diffusion, causing hypoxemia.
  • Also, the fluid decreases the effectiveness of surfactant(dilutes it), leading to a difficulty in expanding the lungs, leading to lung collapse.
  • Capillaries can rupture w/ the high pressure, leading to blood tinged sputum (Hemoptysis)
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11
Q

Etiology of Pulmonary Edema

A

Can be caused by many primary conditions:
1)Left sided CHF: b/c of backup flow/congestion

2) Hypoprteinemia: Low plasma protein in the blood that reduced osmotic pressure
3) Tumours: Interrupts blood flow and also interrupts lymphatic drainage (Lymphedema)
4) Blocked Lymphatic drainage
5) Inhalation of toxic gas: Leads to inflammation response and can cause trauma to the capillaries (increased capillary permeability)

The cause can also be idopathic.

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12
Q

S/s of Pulmonary Edema

A

Mild:

  • Cough
  • Orthopnea
  • Crackles

Moderate/Advanced:

  • Hemoptysis
  • Labored breathing d/t difficulty w/ lung expansion
  • Feeling of drowning b/c of fluid in alveoli
  • Hypoxemia increases b/c of decreases gas exchange
  • Cyanosis develops when advanced
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13
Q

Treatment of Pulmonary Edema

A

1) Fix the cause of edema!
2) Diuretics to remove fluid from lungs
3) O2 diffusion –> increases concentration gradient.
4) Can give surfactant to help increase lung expansion.

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14
Q

What is a Pulmonary Embolism?

A
  • A clot that obstructs the pulmonary artery or a branch of it, blocking the flow through the lung tissue.
  • Most clots originate from DVT’s
  • The lungs are the first site where the arteries are narrow enough to become occluded by the thrombus.
  • Leadings cause of death in hospitals, developing quickly –> biggest post sx complicaton.
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15
Q

Patho of Pulmonary Embolism

A

It depends on the size and the location of obstruction.

-Infarction blocks one segments of the lungs and the pleural membrane in that area.

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16
Q

Patho: Three different types of emboli:

A

1) Small emboli:
- Usually silent/asymptomatic
- Multiple small emboli can result in an effect equal to one large emboli

2) Moderate emboli:
- Can cause respiratory impairment b/c fluid and blood fill the alveoli of the involved area
- Reflex vasoconstriction occurs, increasing the pressure in the blood vessels.

3) Large emboli:
- Loosely defined as impacting 60% totlal or more of the lung tissue
- Results in increased resistance in the pulmonary circulation,
- Affects the cardiovascular system, leading to right sided heart failure and decreased CO (Cor pulmonale)
- Sudden death often results.

17
Q

Etiology of a Pulmonary Embolism

A

DVT:
-Risk factors include: Immobility, trauma, sx, childbirth b/c lots of pressure on the legs, CHF(increased pressure damaging vessels/Artheromas), hypercoaguability, cancer.

Other Emboli:

  • Fat emboli can be releasedfrom the bone marrow following a fracture
  • Vegetations from endocarditis
  • amniotic fluid emboli from placental tears
  • tumor cell emboli or air emboli
18
Q

S/s of Pulmonary Emboli

A

Small Emboli:
-Transient chest pain, cough, dyspnea

Larger Emboli:

  • Chest pain that is increased w/ coughiing or deep breathing, tachyonea, dysnpea.
  • Later appearance of hemoptysis and fever
  • Hypoxia creates pallor, restlessness, anxiety, and tachycadria

Massive Emboli:
-Crushing chest pain, low BP, rapid and weak pulse, loss of consciousness.

Fat Emboli:
-Develops acute respiratory distress, petechial rash onthe trunk and neurological signs including confusion and disorientation.

19
Q

Tx of Pulmonary Emboli

A
  • Give O2
  • Thrombolytic/Fibrinolytic therapy (these may not be so effective for large DVT)
  • Try to prevent formation of a DVT: Incr. movement, diet, quit smoking.
  • If DVT develops, bed rest!
20
Q

What is Acute Respiratory Distress Syndrome?

A

A.k.a “Adult Respiratory Distress Syndrome”

  • Onset usually occurs 1-2days following a precipitating event.
  • May be associated w/ multiple organ dysfuntion.

-Affects many people a year, where about 50-60% of them die despite intensive care interventions.

21
Q

Patho of Acute Respiratory Distress Syndrome

A

Damage to alveoli and/or capillaries –>
Incr. pulmonary HTN(congestion) –>
Decreases elasticity and expansion
(can’t expand = can’t ventilate very well)/decreased lung compliance –>
Decrease in ventilation – perfusion coupling –> Further damage to lung tissues –>
Necrosis , fibrosis, complications (Irreversible)

1) Injury to the alveolar wall and capillary membrane
2) Results in incr. permeability of cap wall = incr. fluid and protein in the interstitial space and alveoli and damage to the surfactant producing cells = decr. surfactant
3) Causes a decr. in O2 diffusion, reduced blood flow to the lungs, difficulty expanding lungs and diffuse atelectasis.
4) Lung volumes decrease
5) Damage increases as proteases (Protein degrading enzymes) are released by arriving neutrophils
6) Hyaline membranes (makes alveoli thicker) form, platelets aggregate and microthrombi develop in the pulmonary circulation.
7) If the pt survives, the lungs will contain necrotic regions and fibrosis.

Predisposed to pneumonia (b/c of fluid and pus is alveoli) and CHF (b/c the hearts won’t get as much oxygenated blood leading to pulmonary HTN) as complications.

22
Q

Etiology of Acute Respiratory Distress Syndrome

A
  • Severe or prolonged shock can cause ARDS as it leads to prolonged ischemia
  • Inhalation of toxic chemicals or smoke (workplace)
  • Excessively high oxygen concentration in the lungs.
  • Severe viral infections
  • Toxins from systemic infections
  • Fat emboli
  • Aspiration of highly acidic fluids (causing damage to the alveoli)
  • Lung trauma
  • Cancer
  • Pancreatitis
23
Q

S/s of Acute Respiratory Distress Syndrome

A

Onset:

  • Dysnpea
  • Rapid and shallow resps (b/c of loss of complicance)
  • Incr. HR
  • Decr. PO2 as evidenced by arterial gases

Progression:

  • Crackles
  • Productive cough
  • Frothy sputum
  • Cyanosis
  • Lethargy
  • Confusion
  • Respiratory and metabolic acidosis
24
Q

Tx of Acute Respiratory Distress Syndrome

A
  • Supply oxygen to vital organs and provide supportive care until the condition causing the patho problem has been reversed
  • Lung need a chance to heal
  • Assisted ventilation using high lvl of O2 are required to overcome the hypoxia.
  • Positive end-expiratory breathing may be used to assist the re-inflation of collapsed areas of lungs and increase the match of ventilation and perfusion.
25
Q

What is Respiratory Failure?

A

Can be the end result of many pulmonary disorders

Indicated when either:

  • PO2 drops below 50mmHg (normal 80-100
  • PCO2 is higher than 50mmHG (normal 30-40)

These values cannot even meet the metabolic needs of the body at rest.

26
Q

Etiology of Respiratory Failure

A
  • COPD conditions
  • Underlying chronic disorders w/ a current acute tissue
  • Trauma
  • Neuromuscular diseases(Ex: ALS) b/c the resp. muscles can’t work properly/they fail.
27
Q

What are some conditions that can cause Respiratory Failure?

A

Conditions that affect blood flow into the lungs:
-Pulmonary Embolism: blocks blood flow and causes lung damage

Conditions that affect the nerves and muscles that control breathing:

  • Muscular dystrophy: Amyotrophic lateral sclerosis
  • Spinal cord injuries

Conditions that affect the areas of the brain that control breatihing:

  • Stroke
  • Drug/alcohol overdose

Conditions that affect the flow of air in and out of the lungs:

  • COPD
  • Cystic Fibrosis (thick mucus in the airways)

Conditions that affect gas exchange in the alveoli

  • ARDS
  • Pneumonia (airway filled w/ fluid and pus)
28
Q

S/s of Acute Respiratory Distress Syndrome

A

-Rapid,shallow and labored respirations

-General signs of hypoxia and hypercapnia:
Headache
Tachycardia
Lethargy
Confusion
29
Q

Tx of Acute Respiratory Distress Syndrome

A

Resolve the primary problem in an effort to maintain resp function (if possible)

Pathophysiology (7 decks)

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