Pulm. ARDS + PH+ cor pulmonale (09-29) (2) Flashcards
UW. ARDS. Risk factors?
Infection, trauma, massive transfusion, acute pancreatitis
UW. ARDS. Patho. Lung injury –>?
fluid/cytokine leakage into alveoli
UW. ARDS. Patho. leaky capillaries ->
crushes alveoli
UW. ARDS. Patho. O2 barier?
Bigger diffusion barrier to oxygen.
Less surface area.
UW. ARDS. Patho - mcc?
Sepsis is associated with cytokines (IL-1, IL-6, TNF) which can activate inflammatory
cells that injure alveolar and capillary epithelium
UW. ARDS. Patho. accumulation of protein fluid –>
Protein rich fluid accumulates in alveoli which disrupts surfactant which leads to alveoli collapse.
UW. ARDS. Patho. V/Q mismatch.
.
UW. ARDS. clinical presentation?
Sick.
Hypoxemic.
Near drowning or septic shock.
PaO2/FiO2 (oxygen in blood/alveolar oxygen) <300.
Increased A-a gradient.
UW. ARDS. diagnosis. xray?
pulmonary edema and bilateral alveolar infiltrate.
UW. ARDS. diagnosis. PCWP (wrong).
.
UW. ARDS. diagnosis. what to do to rule out CHF?
BNP and cardio echo
UW. ARDS. diagnosis. echo findings, PCWP?
Normal or elevated LV function in ARDs.
PCWP is decreased or normal.
UW. ARDS. treatment?
Mechanical ventilation very important (yra algoritmas)
UW. ARDS. DPV. what are important measures of oxygenation?
FIO2 and PEEP is an important measure of oxygenation.
UW. ARDS. DPV. what affect CO2?
Respiratory rate and
tidal volume affect PaCO2
UW. ARDS. DPV. what ,,ventilation”?
Low tidal volume ventilation (LTVV)
UW. ARDS. DPV. what volume?
(6ml/kg of ideal body weight)
UW. ARDS. DPV. LTVV decreases
the likelihood of over distending alveoli and provoking barotrauma due to
high plateau pressures.
.
UW. ARDS. DPV. oxygenation. what starting FiO2, mechanism?
Adequate oxygenation: increasing FiO2 by the ventilator improves oxygenation; more than 60% is associated with oxygen toxicity but they are often provided high FiO2 after intubation and then weaned to below 60%.
UW. ARDS. DPV. PEEP mechanism?
Increasing PEEP also improves oxygenation by preventing alveolar collapse at the end of expiration; thereby decreasing shunting and the work of breathing.
UW. ARDS. DPV. what PEEP maybe nedded?
PEEP levels up to 15-20 cm of H20 might be necessary to maintain
oxygenation.
UW. ARDS. DPV. what is the goal of PO2?
The goal is PaO2 between 55 and 80 mmHg and an SpO2 between 88 and 95%.
UW. ARDS. DPV. prone and supine? duration
Prone for 16 hours, supine for 8 hours for mild disease and early in the course of
disease.
UW. ARDS. DPV.
Intubation –> Initial settings?
Oxygenation: FiO2 100 proc, PEEP 5
Ventilation: Vt 6ml/IBW, RR 14-18
UW. ARDS. DPV.
Intubation –> Initial settings –> Adjust
OXYGENATION
or VENTILATION.
.
UW. ARDS. DPV.
Adjust OXYGENATION –> PaO2 > 90 (hyperoxia)
Decr. FiO2
UW. ARDS. DPV.
Adjust OXYGENATION –> PaO2 < 60 (hypoxia)?
Incr. PEEP
UW. ARDS. DPV.
Adjust VENTILATION –> incr. PaCO2 and pH < 7,25 –> ?
Incr. RR
incr. Vt as last resort
UW. ARDS. DPV.
Adjust VENTILATION –> decr. PaCO2 and pH >= 7,45 –> ?
decr. Vt
decr. RR
incr. sedation as last resort
UW. ARDS. DPV. Avoid alveolar overdistension.
Evaluate lung compliace. how to do that?
measure Pplat with inspiratory hold
*inspiratory hold - pause ventilator briefly after TV is delivered and measure pressure required to hold the lungs at distension on current setting
Goal Pplat =< 30 cmH2O: decr. Vt and/or adjust PEEP
UW. ARDS.
Note: noncardiogenic pulmonary edema can also occur when a patient has upper airway obstruction that leads to a large negative intrathoracic pressure (inspiration against obstruction).
.
UW. ARDS. supportive care.
1. treat underlying cause, eg sepsis.
.
UW. ARDS. supportive care.
2. prevent iatrogenic harm ->?
Negative fluid balance, timely extubation (eg minimize sedation)
UW. ARDS. supportive care.
3. coritcosteroids?
+/-
select patients with moderate-severe early ARDS
UW. ARDS. prognosis?
Mortality: 40 proc. in hospital, mostly due to multiorgan failure
Morbidity: 50proc. with chronic cognitive impairment and physical debility, 25 proc. with chronic pulmonary dysfunction (restriction and decr. DLCO)
UW. PH. Classification. group 1?
Pulmonary arterial hypertension: idiopathic or due to drugs, HIV, connective tissue disease
UW. PH. Classification. group 2?
Due to left-sided heart disease
UW. PH. Classification. group 3?
chronic lung disease (eg COPD, ILD) or hypoxemia
UW. PH. Classification. group 4?
due to chronic thromboembolic disease
UW. PH. Classification. group 5?
due to other causes (eg hematologic, sarcoidosis)
UW. PH. what pressure?
> =25 mmHg or more at rest
UW. PH.
Idiopathic
Secondary
Systemic sclerosis and CREST syndrome; hyperplasia of the intimal smooth muscle
layer.
Restrictive lung disease; restrictive pattern on PFTs.
Bronchiectasis; obstructive pattern on PFTs.
Left sided heart failure.
.
UW. PH. symptoms?
dyspnea, fatigue/weakness,
exertional angina, syncope
abdominal distension/pain
UW. PH. diagnosis? 2 methods
cardio echo - can measure pulmonary artery pressure
most accurate - right heart catheterization
UW. PH. symptoms. sounds
Loud P2, right-sided 3
Pansystolic murmur of tricuspid regurgitation
UW. PH. symptoms. chest lifts?
left parasternal lift, right ventricular heave
UW. PH. symptoms. general symptoms?
JVD, ascites, peripheral edema, tender hepatomegaly
UW. PH. drugs treatment - in symptomatic idiopathic (group1).
in other groups - treat underlying cause
.
UW. PH. treatment what drugs?
Endothelin receptor antagonist (bosentan)
PDE-5-inhibitor (sildenafil), and/or
prostanoids (apoprostenol).
UW. PH. what does endothelin? pathway.
endotelin-1 joins to endothelin receptor –> vasoconstriction and incr. proliferation of smooth muscles.
Bosentan - inhibitor
UW. PH. what does NO? pathway.
NO –> cGMP –> vasodilation and decr. proliferation.
PDE-5 inhibitors and Nitrates have positive effect on cGMP.
UW. PH. what does prostacyclin? pathway.
prostacyclin –> cAMP –> vasodilation and decr. proliferation
Prostacyclin analogues, ar cia tas pats kas prostanoids (apoprostenol).?
UW. PH. Early symptoms?
dyspnea, weakness, fatigue
UW. PH. Late symptoms?
chest pain, hemoptysis, syncope, hoarseness (due to compression of recurrent laryngeal nerve)
UW. PH. right ventricular failure late in disease.
.
UW. PH. diagnosis (very well know methods)?2
xray:
Enlargement of pulmonary arteries with rapid tapering of the distal vessels (pruning)
Enlargement of right ventricle
ECG - right axis deviation (due to right ventricular strain and hypertrophy)
UW. PH. untreated leads to cor pulmonale
.
UW. cor pulmonale. definition?
Right-sided heart failure (RHF) from pulmonary hypertension
UW. cor pulmonale.
RHF due to left-sided or congenital heart disease is NOT considered cor pulmonale.
.
UW. cor pulmonale.
diagnosis? 3
xray
ECG
Right heart catheterization (gold standard for diagnosis)
UW. cor pulmonale. diagnosis gold standard?
Right heart catheterization (gold standard for diagnosis)
UW. cor pulmonale.
xray - whats seen?
i. Enlarged central pulmonary arteries
ii. Loss of retrosternal air space due to right ventricular hypertrophy
UW. cor pulmonale.
ecg changes?
i. Right axis deviation
ii. RBBB
iii. Right ventricular hypertrophy
iv. Right atrial enlargement
UW. cor pulmonale.
Right heart catheterization (gold standard for diagnosis), whats seen?
i. incr. CVP
ii. incr. Right ventricular end-diastolic pressure
iii. inc.r Mean pulmonary artery pressures (>= 25mm Hg at rest)
UW. cor pulmonale. treatment.
a) optimizing right ventricular dynamics (preload, afterload, and contractility)?
i. Supplemental oxygen
ii. Diuretics
iii. Treatment of underlying etiology
UW. cor pulmonale. treatment.
b) what for severe decompensation?
IV inotropes are given for severe decompensation