Pulm Vascular Disorders

Question 1

What is pulmonary congestion?

Answer 1

congestion within the blood VESSEL driving fluid out of vessels into interstitial spaces – is NOT BLOOD IN THE LUNGS!

•Not correct to say fluid in the lungs, because there is always fluid there (thin film essential for gas exchange)

Question 2

What is pulmonary edema?

Answer 2

Accum of fluid INSIDE the alveoli

Question 3

Et of pulmonary edema?

Answer 3

• Usually left sided heart failure 
• Non cardiogenic (not cardiac related causes): 
 - IV Fluid overload
- Smoke inhalation (
- Aspiration
- IV drug abuse

Question 4

How does smoke inhalation cause pulm edema?

Answer 4

not from smoking but rather from a fire…have toxic fumes in this smoke that will bring about inflm, alter permeability of vessels, which permits fluid to move into the alveoli)

Question 5

How does IV drug abuse lead to pulm edema?

Answer 5

because inc permeability of vessels + depresses CNS (which controls resp and circ…impacting exchange of fluid between blood and instersitital spaces)

Question 6

Patho of pulm edema?

Answer 6

`Fluid from blood to IS to alveoli → dec resp function (as longer diffusion distance)

• In order to move across for gas exchange, O2 and CO2 need to be able to dissolve into the fluid between the capillary and the alveoli…with PE, fluid is added into this space → expanded diffusion distance + also taking up space that air would otherwise occupy in alveoli

Question 7

Manifestations of pulm edema?

Answer 7

• Cough – productive (frothy + blood tinged)
• Dyspnea
• Dec compliance (d/t presence of fluid)
• Crackles

Question 8

Why is cough frothy + blood tinged with pulm edema?

Answer 8

frothy c/b mixing air and fluid

blood tinged if damage to blood vessels

Question 9

Tx of pulm edema?

Answer 9

• Resp support (while find cause)

* Cause – eg: inc heart fx

Question 10

What is pulm embolism?
How often does it reccur?
Is it serious?

Answer 10

• Thrombus in the pulmonary vessel (will be an ARTERY)
• Potentially lethal – if is one of larger arteries, will be about ~1/3 death rate
• MI is same thing in pulmonary circuit
• 10% recurrence rate (problem returns at later date)

Question 11

Outline pulmonary circulation

right and left circuits, where is oxygenated, etc

Answer 11

R side heart 
Pulm arteries (deoxy)
Pulm cap bed
Pulm veins (oxy)
L side heart 
Systemic circuit.

Question 12

Et of pulm embolism?

Answer 12

• Usually from DVT (from iliac, popliteal, or femoral vein)
• Other emboli:
  1) Fat
  2) Air
  3) Amniotic fluid

Question 13

Where does a fat embolism come from?

Answer 13

could come from bone marrow if you have fracture (sever blood vessels which have marrow adjoining, fat enters circulation here)

Question 14

Where would air embolism come from?

Answer 14

IV, injection

Question 15

How does emboli occur from amniotic fluid?

Answer 15

during birthing process, these membranes rupture and release amniotic fluid….also during labour and birth, vessels are severed and burst…
• Here talking about the particulate matter in the fluid, not the fluid itself

Question 16

What is a “saddle” embolus?

Answer 16

embolus settles in “saddle” formed by bifurcation of the pulmonary artery

Question 17

Patho of pulm embolism

Answer 17

• DVT → embolus → thrombus in arterial bed → impaired perfusion
• Ventilation : perfusion imbalance → hypoxemia (this is small issue in comparison to thrombus)
• Platelets degranulate (mediators released) → bronchial and pulmonary artery constriction (which worsens problem) → hemodynamic instability
• Reflexive bronchoconstriction
• Dec in cardiac output
• L/o surfactant → atelectasis
• Right-sided heart failure possibly results

Question 18

What is hemodynamic instability?

Answer 18

changes in blood volume, pressure, and flow

Question 19

Why does reflexive bronchoconstriction occur with pulm embolism?

Answer 19

no benefit, is consequence of sympathetic response

Question 20

Why dec CO with pulm embolism?

Answer 20

d/t thrombus occluding pulmonary artery so little blood returning to the left side of the heart

Question 21

WHy does l/o surfactant occur with pulm embolism?

Answer 21

o Why does this occur? 1) Any secretion from a gland requires adequate perfusion; 2) Even if perfusion is partial or relatively adequate, whenever there is some impact in perfusion, you have ischemic damage to these cells

Question 22

Why RSHF possible with pulm embolism?

Answer 22

Because is pumping against increased resistance → will hypertrophy + fail…then LSHF could follow (but generally person will die before this occurs if there is not intervention)

Question 23

Manifestations of pulm embolism?

Answer 23

• Based on size and site
• Usually: chest pain, tachypnea, dyspnea
- Tachycardia

Question 24

WHy chest pain and tachypnea with pulm embolism?

Answer 24

o Chest pain d/t Ischemia
o Tachypnea d/t resp system working in concert with cardio system…one is failing, the other is attempting to compensate. Also may have bronchoconstriction

Question 25

Why tachycardia with pulm embolism?

Answer 25

compensatory response for dec’d CO

Question 26

Dx of pulm embolis?

Answer 26

- Hx + px (differentiate from MI) - ABG (acid/base, etc) - LDH3 (lactate dehydrogenase) - Lung scan (131 I-HSA, IV) - Ct, CXR - Pulm angiogram

Question 27

LDH3 ?

Answer 27

Lactate Dehydrogenase, enzyme released when there is damage to the lung tissue (d/t infarction from ischemia) o #3 says is subset of other LDH…like subclasses of CKMB, BB, etc.

Question 28

Lung scan (131 I-HSA, IV)

Answer 28

HAS is marked albumin, protein is labeled with Iodine 131; a radio isotope used to tag compounds; o Will show you if you have a larger obstruction o Albumin marked with isotope injected o This is non invasive procedure

Question 29

Tx of pulm embolism?

Answer 29

* STAT treatment improves prognosis * Once dissolved thrombus, need to also address the platelets “making merry” – stop the party! * Anticoagulants & thrombolytics * Maintain cardio-pulmonary function (avoids shock) * Treat DVT

Question 30

What is pulm HTN?

Answer 30

• Sustained pressure inc in pulm circuit (>25 mmHg; normal ~15) • Not systemic hypertension • Is like portal hypertension in that is confined to the pulmonary system • Is pathologic htn, so need to note that it’s prolonged (unlike physiologic hypertension experienced during exercise) • Pulmonary vasoconstriction → inc pressure + other problems outlined in etiology

Question 31

Is pulm circuit a high pressure system?

Answer 31

o Is low pressure, low resistance circuit → has many paths as vessels disseminate, so as progress into capillary beds, pressure drops • If cardiac output increases, will be slight increase in pressure of the circuit, but should not cause any significant inc in pressure (vessels should be able to handle that inc)

Question 32

Et of pulmonary HTN?

Answer 32

2ndry to cardiac & pulm problems 3 categories/kinds of problems: 1) Inc in pulm volume (eg: cardiac septal defects) 2) Hypoxemia 3) Inc pulm venous P (eg: left ventricular dysfunction)

Question 33

What occurs in septal defects?

Answer 33

**REVIEW FETAL CIRC PATTERN Fetal blood not cycled through lungs; this is partially achieve by having opening of septum between RA and LA so blood channeled through this and out through aorta…. i. Septal defect: incomplete closure means more blood is being sent through the lungs

Question 34

How does hypoxemia cause pulm HTN?

Answer 34

a. If tissue is deprived of oxygen, the response of the vessels in vasodilation → in lungs, would you expect the same response? For other tissues, this oxygen comes FROM the lungs. Now if you have hypoxemia within the lung tissue itself – response of lung vessels now is actually vasoconstriction because it’s trying to localize the accumulation of CO2, rather than causing widespread hypoxemia

Question 35

How does LV dysfx cause pulm HTN?

Answer 35

Have left sided failure…pooling of blood in LV, then LA, then pulmonary circuit…with vol increase comes inc in pressure

Question 36

Manifestations of pulm HTN

Answer 36

* DO NOT NEED TO EXPLAIN • Dyspnea, syncope + chest pain on exertion • Those of RSHF (if does result in HF) • On chest xray will see 2 things if is severe: 1) RV hypertrophy 2) Distended pulm arteries • Fatigue – gen systemic manifestation

Question 37

Tx of pulm HTN

Answer 37

* Is very difficult! * Cause * Vasodilators – Need to take into consideration that these are not specfic to pulm vessels, will cause systemic vasodilation * Poor prognosis if severe

Question 38

What is ARDS?

Answer 38

Acute Resp Distress Sydrome •Severe damage to alveolar + cap walls - Acute onset, rapidly progresses (d/t fire, drowning, etc) - 40-60% mortality

Question 39

Alternative ways that ARDS is named? Which are acceptable according to Ahmed?

Answer 39

* Sometimes see “acute” replaced with “adult”….this is not accurate, Ahmed says you should correct this! * May see described as “wet lung” but this is also wrong because is not only due to drowning * May also see “post traumatic lung”, which Ahmed says is acceptable

Question 40

Etiology of ARDS?

Answer 40

``` See chart 29-2 (pick those we know) Egs: • Aspiration (ex: gastric contents) • Excessive smoke inhalation (from fire) • Fat embolus • Septicemia • Drugs: cocaine, heroin • Severe burns (and other trauma such as fat embolism + chest trauma) • Near drowning ```

Question 41

Pathophysiology of ARDS

Answer 41

SEE FIG 29-13 • Lung trauma → neutrophil influx (with vasodilation + inc cap perm)→ activated neutrophils release free radicals, phospholipids, and proteases (+ leukotrienes + PAF in diagram)→ endothelial & alveolar damage → inc perm → accum of inflammatory and non-inflm components ( efflux of proteins, cells & fluids into IS & alveoli) → edema→ dec in compliance and impaired gas exchange • Surfactant deficiency & inactivation → atelectasis * Thick protein and cell rich exudate lines alveoli → no gas exchange * Impervious hyaline membrane lines alveoli • Profound hypoxemia

Question 42

How is the edema that occurs in ARDS esp bad?

Answer 42

has fluid and non-fluid components…cellular debris, proteins (both albumin and proteins involved in inflm), etc. – b/c o this, is far worse than pulmonary edema because can’t simply take away the fluid, these other components get left behind

Question 43

Is the hyaline membrane that lines the alveoli in ARDS a membrane in the histological sense? Is this like hyaline cartilage?

Answer 43

No and no.

Question 44

Why do you see surfactant deficiency and inactivation in ARDS?

Answer 44

D/t alveolar cell damage (is what text says)...double check this?

Question 45

Manifestations of ARDS

Answer 45

Not complete list... - Acute onset resp distress – within minutes of person in fire, drowning - Dyspnea - Tachypnea - Profound hypoxemia - Early resp alkalosis - Late metb acidosis - Diffuse consolidation

Question 46

Is tachypnea a useful compensation method in ARDS?

Answer 46

as damage progresses and gas exchange becomes impossible, this is no longer useful (movement from compensation to decompensation)

Question 47

Why early resp alkalosis in ARDS?

Answer 47

o Tachypnea, CO2 + H20 → H2CO3→ HCO3- + H+ | o Exhaling CO2 now driving equation to the right…

Question 48

What kinds of acids indicate resp acidosis? Metb acidosis?

Answer 48

carbonic acid is VOLATILE acid…this means is respiratory – metabolic is fixed acids

Question 49

Why late metb acidosis in ARDS?

Answer 49

o Are going into anaerobic metabolism because severe deficiency of oxygen, producing lactic acid

Question 50

Why diffuse consolidation with ARDS?

Answer 50

exudate with fluid in it solidifies causing consolidation

Question 51

Tx of ARDS?

Answer 51

* Early intervention to achieve better prognosis * Reverse cause * Respiratory support – from O2 admin to putting on mechanical ventilator * Complications