Pulm Vascular Disorders Flashcards
What is pulmonary congestion?
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)
What is pulmonary edema?
Accum of fluid INSIDE the alveoli
Et of pulmonary edema?
• Usually left sided heart failure • Non cardiogenic (not cardiac related causes): - IV Fluid overload - Smoke inhalation ( - Aspiration - IV drug abuse
How does smoke inhalation cause pulm edema?
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)
How does IV drug abuse lead to pulm edema?
because inc permeability of vessels + depresses CNS (which controls resp and circ…impacting exchange of fluid between blood and instersitital spaces)
Patho of pulm edema?
`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
Manifestations of pulm edema?
- Cough – productive (frothy + blood tinged)
- Dyspnea
- Dec compliance (d/t presence of fluid)
- Crackles
Why is cough frothy + blood tinged with pulm edema?
frothy c/b mixing air and fluid
blood tinged if damage to blood vessels
Tx of pulm edema?
- Resp support (while find cause)
* Cause – eg: inc heart fx
What is pulm embolism?
How often does it reccur?
Is it serious?
- 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)
Outline pulmonary circulation
right and left circuits, where is oxygenated, etc
R side heart Pulm arteries (deoxy) Pulm cap bed Pulm veins (oxy) L side heart Systemic circuit.
Et of pulm embolism?
- Usually from DVT (from iliac, popliteal, or femoral vein)
- Other emboli:
1) Fat
2) Air
3) Amniotic fluid
Where does a fat embolism come from?
could come from bone marrow if you have fracture (sever blood vessels which have marrow adjoining, fat enters circulation here)
Where would air embolism come from?
IV, injection
How does emboli occur from amniotic fluid?
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
What is a “saddle” embolus?
embolus settles in “saddle” formed by bifurcation of the pulmonary artery
Patho of pulm embolism
- 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
What is hemodynamic instability?
changes in blood volume, pressure, and flow
Why does reflexive bronchoconstriction occur with pulm embolism?
no benefit, is consequence of sympathetic response
Why dec CO with pulm embolism?
d/t thrombus occluding pulmonary artery so little blood returning to the left side of the heart
WHy does l/o surfactant occur with pulm embolism?
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
Why RSHF possible with pulm embolism?
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)
Manifestations of pulm embolism?
• Based on size and site
• Usually: chest pain, tachypnea, dyspnea
- Tachycardia
WHy chest pain and tachypnea with pulm embolism?
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
Why tachycardia with pulm embolism?
compensatory response for dec’d CO
Dx of pulm embolis?
- Hx + px (differentiate from MI)
- ABG (acid/base, etc)
- LDH3 (lactate dehydrogenase)
- Lung scan (131 I-HSA, IV)
- Ct, CXR
- Pulm angiogram
LDH3 ?
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.
Lung scan (131 I-HSA, IV)
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
Tx of pulm embolism?
- 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
What is pulm HTN?
• 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
Is pulm circuit a high pressure system?
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)
Et of pulmonary HTN?
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)
What occurs in septal defects?
**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
How does hypoxemia cause pulm HTN?
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
How does LV dysfx cause pulm HTN?
Have left sided failure…pooling of blood in LV, then LA, then pulmonary circuit…with vol increase comes inc in pressure
Manifestations of pulm HTN
- 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
Tx of pulm HTN
- 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
What is ARDS?
Acute Resp Distress Sydrome
•Severe damage to alveolar + cap walls
- Acute onset, rapidly progresses (d/t fire, drowning, etc)
- 40-60% mortality
Alternative ways that ARDS is named? Which are acceptable according to Ahmed?
- 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
Etiology of ARDS?
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
Pathophysiology of ARDS
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
How is the edema that occurs in ARDS esp bad?
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
Is the hyaline membrane that lines the alveoli in ARDS a membrane in the histological sense?
Is this like hyaline cartilage?
No and no.
Why do you see surfactant deficiency and inactivation in ARDS?
D/t alveolar cell damage (is what text says)…double check this?
Manifestations of ARDS
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
Is tachypnea a useful compensation method in ARDS?
as damage progresses and gas exchange becomes impossible, this is no longer useful (movement from compensation to decompensation)
Why early resp alkalosis in ARDS?
o Tachypnea, CO2 + H20 → H2CO3→ HCO3- + H+
o Exhaling CO2 now driving equation to the right…
What kinds of acids indicate resp acidosis? Metb acidosis?
carbonic acid is VOLATILE acid…this means is respiratory – metabolic is fixed acids
Why late metb acidosis in ARDS?
o Are going into anaerobic metabolism because severe deficiency of oxygen, producing lactic acid
Why diffuse consolidation with ARDS?
exudate with fluid in it solidifies causing consolidation
Tx of ARDS?
- Early intervention to achieve better prognosis
- Reverse cause
- Respiratory support – from O2 admin to putting on mechanical ventilator
- Complications
