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253-Green Patho > Respiratory- Vascular > Flashcards

Respiratory- Vascular Flashcards

1
Q

What is Pulmonary Edema

A

Accumulation of fluid in the alveoli

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2
Q

What problems does fluid accumulation cause in Pulmonary Edema? (2)

A

Increase of diffusion distance, decreasing compliance (less space for air)

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3
Q

What are the Cardiac and Non Cardiogenic etiologies for Pulmonary Edema

A

• Usually LHF

• Non cardiogenic
o IV fluid overload 
o Smoke inhalation (inflm inducing)
o Aspiration
o IV drug abuse (Narcotics- inc cap permeability, and …missed something in class)
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4
Q

Basic Patho of Pulmonary Edema?

A

• Fluid from blood to Interstitial Space to alveoli -> Dec resp. Fx

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5
Q

MNFTS of Pulmonary Edema?

A
  • Dyspnea
  • Productive Cough (frothy, maybe blood tinged…d/t cough)
  • Dec Compliance
  • crackles
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6
Q

What is the difference in MNFTS of Pulmonary edema versus a Pulmonary Effusion

A

Pulmonary Edema has a productive wet cough, Pulmonary effusion is a dry cough.

Though both will irritate of alveoli

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7
Q

Tx of Pulmonary Edema

A

• Resp support
• Cause (identify and treat)
o (Eg inc heart fx)

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8
Q

What is a Pulmonary Embolism?

A

Embolus in a pulmonary vessel

THROMBUS! (stationary vs embolism moving)

OR
o Fat (r/t fracture)
o Air (inotrogenic)
o Amniotic fluid (particulates)

(Notes and card will generally be referring to a Thrombus, since almost all embolisms are of this type)

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9
Q

What is the recurrence rate of a pulmonary embolism?

A

10% recurrence rate

I.e. if you’ve had one, what are the chances you’ll get another

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10
Q

Where are thrombi generally coming from that end up in pulmonary circuit

A

Iliac, popliteal or femoral veins

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11
Q

Patho of Pulmonary Embolism?

A
  • DVT -> embolus -> thrombus in arterial bed -> impaired perf
  • Ventilation: perfusion imbalance -> hypoxemia
  • Platelets degranulate -> (mediators) -> bronchial and pulmonary artery constriction -> hemodynamic instability
  • Reflexive Bronchoconstriction
  • Reduced CO output (r/t dec return to left side)
  • Loss of surfactant (reduce 02 to to secretory cells means dec secretion) -> atelectasis
  • RHF (d/t increase workload)
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12
Q

What are the risk factors for thrombus formation?

A

Virchows Triad- stasis, hypercoagulability, venous endothelial injury

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13
Q

MNFTS of Pulmonary Embolism

A

• Based on size and site
• Usually:
o Chest pain, tachypnea, dyspnea (d/t hypoxia)
• Tachycardia to inc CO (Weak and rapid pulse)

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14
Q

Dx of Pulmonary embolism?

A
  • Hx, Px
  • ABG’s
  • LDH 3
  • Lung Scan
  • Chest CT
  • Pulmonary angiogram (Evasive, but more specific)
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15
Q

What is LDH3 and why use it to Dx pulmonary Embolism

A

Lactate Dehydrogenase – enzyme present in high quantities in lung tissue

Works as serum marker for tissue damage in that area

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16
Q

How does a Lung scan work?

AKA Ventilation-Perfusion scan

A

HSA (human serum albumin) is Pushed IV
(just to fill vessels?)

Iodine radioactively marked 131 is inhaled.

You then watch radioactive Iodine with gamma camera distribute into circulatory system and look for blockages.

17
Q

Tx for Pulmonary Embolism

A
  • Stat tx provides better prognosis
  • Anticoagulant and thrombolytics (fat or air would be different)
  • Cardiopulmonary support (avoid shock)
  • Treat DVT issues
18
Q

What is Pulmonary HTN

A

• Sustained inc of pressure in pulmonary circuit

o (> 25mmHg : Normal is ~15)

19
Q

What characterizes the pulmonary circuit and what affects pressure in the system

A

Low pressure system.

If CO increases -> Minimal increase in pulmonary pressure

Pulmonary vasoconstriction -> inc in pressure

20
Q

What is Pulmonary HTN often secondary to?

A

Secondary to cardiac and pulmonary problems

21
Q

Describe 3 distinct etiologies that would lead to P HTN

A

o Increase in pulmonary volume (eg cardiac septal defects)
• Blood from LV into RV

o Hypoxemia
• Vasoconstriction in lungs limits CO2 to rest of body (Hypoxia causes vasodilation in every other tissue but the lungs… In pulmonary circuit = vasoconstriction)

o Inc pulmonary venous pressure (ex congestion from Left sided heart failure)

22
Q

MNFTS of P HTN

A

• Dyspnea, syncope and chest pain on exertion
• Those of R sided Heart Failure (pumping against increased resistance)
• Fatigue
• On chest Xray
o Distention of pulmonary artery
o Hypertrophy of Right Ventricle

23
Q

What is Syncope?

A

Temporary loss of consciousness r/t drop in Bp

24
Q

Tx for P HTN?

A
  • Cause (Identify and Treat)
  • Vasodilators (causing systemic issues)
  • Dec in prognosis if severe
25
Q

What is ARDS?

A

Acute Onset Respiratory Distress

Severe damage to alveolar and capillary walls
• Acute onset and progressive
• 40-60% mortality
• inflm response due to injury becomes pathological and inflm debris from impermeable barrier in alveoli

26
Q

What is ARD’s AKA

A

Post Traumatic Lung

The terms- wet lung, Adult RDS are also thrown around but have fallen out of favor

27
Q

Describe some Etiologies of ARD

A

o Aspiration (near drowning, Gastric contents)
o Major smoke inhalation
o Fat embolism (Trauma)
o Septicemia (defenses need to be compromised)
o Drugs (cocaine, heroin)
o Burns

28
Q

Why does debris enter alveoli? ARD

A

Major Inflm or inc cap permeability change allowing fluid, protein, cell debris, platelets and blood cells to move from vascular into alveoli.

29
Q

BASIC Patho of ARD

A

•Lung trauma -> neutrophil influx -> free radicals and Phosopholipids and proteases -> endothelial and alveolar damage -> inc permeability (excessive and pathological, non defense cells move out as well) -> efflux (away from vessels) of proteins, cells and fluid into Interstitial space and alveoli -> edema ( with different components then normal) -> Dec compliance and impaired gas exchange

30
Q

Three major pathological issues present in ARD?

A
  • Surfactant def and inactivation -> atelectasis
  • Thick protein and cell rich exudate lines alveoli (AKA Impervious “Hyaline membrane” -> no gas exchange
  • Profound hypoxemia
31
Q

What is a Hyaline membrane in ARD?

A

Impervious layer (shiny and hard) that lines alveoli

NOTE: This is neither a true membrane or hyaline cartilage

32
Q

MNFTS OF ARDS

A
  • Acute onset resp distress
  • Dyspnea
  • Tachypnea
  • Very high hypoxemia
  • Early Resp alkalosis (r/t to tachypnea) Dumping C02
  • Late metb acidosis (hypoxia -> anaerobic -> lactic acid)
  • Diffuse consolidation
33
Q

Tx of ARD

A
  • Early intervention
  • Reverse cause
  • Extensive Resp support
  • Complications (identify and treat)

253-Green Patho (21 decks)

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