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25 Cards in this Set
- Front
- Back
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Bosentan
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Endothelin receptor antagonist
-blocks ER-A + ER-B-->vasodilation -Tx for class III and IV iPAH |
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Ambrisentan
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Tx for class II-III iPAH
-blocks ER-A |
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Epoprostenol
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Prostanoid-->replaces Prostacyclin
-Class III and Class IV patients |
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Trepostinil
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Class II-->IV iPAH
-site pain problematic |
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Iloprost
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class III and IV iPAH
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Sildenafil
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All classes of PAH
-PDE-5 Inhibitor--> blocks inhibitory effect of PDE-5 on cGMP-->vasodilation |
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Respiratory failure
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PaO2<50mmHg on 50% O2
PaCO2 >50mmHg |
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Acute Respiratory Failure
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pH<7.25: abrupt onset of CW weakness or depression of respiratory system-->increased PCO2
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Chronic Respiratory Failure
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pH approaches 7.40, increased pCO2
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Acute Respiratory Failure Rules
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for every 10mmHg change in pCO2, there is a 0.08 change in pH.
a) PaCO2 40-->50mmHg; pH 7.40-->7.32 b)PaCO2 40-->60mmHg; pH 7.40-->7.24 c.PaCO2 40 -->30mmHg. pH 7.40-->7.48(hyperventilation) |
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Rules for chronic respiratory Failure
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for every 10mmHg change in PaCO2, 0.03 change in pH
1) PaCO2 40-->50; pH7.40-->7.37 2) PaCO2 40-->60; pH 7.40-->7.34 (pH rises slowly in emphysema as lungs no longer have sufficeint alveolar ventilation-->kidney compensates |
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Blood gas interpretation
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Look @ PaO2 first
-will never die of PaCO2 |
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pH 7.33, PaCO2 60
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chronic respiratory acidosis w/ metabolic compensation
-Chronic respiratory failure |
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pH 7.38, PaCO2 48
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Chronic respiratory acidosis w/ metabolic compensation
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pH 7.45, PaCO2 35
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acute respiratory alkalosis
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Signs and symptoms of respiratory Failure
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co2 rises-->vasodilation-->flushed, feel hot, anxious, uncooperative
CNS: headache, somnolence, cloudy conciusness (high cerebral blood floa and high PCO2), restlessness, slurred speech, mood fluctuation (low PaO2), seizures, loss of conciousness, brain damage CV: tachycardia w/ mild hypertension (catecholamine release); bradycardia w/ hypotension when profound Kidney- impaired function, proteinuria, Na+ retention Lung-pulmonary hypertension Lactic acid Metabolic Acidosis |
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ARDS
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-(intrinsic problem within lung)
-not responsive to O2 -noncardiogenic Pulm edema -secondary to pulm capillary endothelial damage |
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ALI
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Acute Lung Injury: less sever form, prelude of ARDS
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ALI vs ARDS
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ALI: PaO2/FiO2=300 or less
ARDS: PaO2/FiO2=200 or less |
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On 100% O2, PaO2 is 90
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-If on 100% O2 and PaO2 is 90: 90/1.00 = 90 (ARDS)
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On 50% O2, PaO2 is 160
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160/0.50 = 320
-->hypoxemia |
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On 50% O2, PaO2 = 110
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110/.50 = 220 = ALI
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ARDS causes
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should be no increase in PCWP
-Sepsis (viral/bacterial)--> inflammatory mediator release -Fat embolism -Aspiration pneumonia -Pancreatitis -Multiple Blood transfusions -Chemical pneumonia |
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ARDS pathophysiology
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-disruption of pulmonary endothelial and epithelial surfaces w/endothelial cell activation
Fluid accumulation = k((Pc-Pif)-sigma(Posm - Posmif)) Increase in k and decrease in Sigma --> fluid accumulation -->recruitment of inflamm cells, activation of coagulation and inhibition of fibrinolysis-->decrease in compliance -fluid in interstitium-->sufactant inactivation |
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Tx ARDS
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1) tx underlyng process
2) Correct hypoxemia a) mechanical ventilation (intubate)w/PEEP -put on diff portion of P/V curve-->open alveoli -very low lung volume-->loss of compliance-->distension of normal compliant airways |
