best: (Crit Care Med 2007;35:2037)
(Clinical Pulmonary Medicine 2004;11(1):40)
Cor pulmonale is pulmonary hypertension in the setting of respiratory disease either acute or chronic, it does not require right heart failure thought that is sometimes a sequelae
Divided into primary, which is idiopathic (PPH or IPH) and secondary, from a cause outside of the lung vasculature.
While acute disease may be reversible, vascular remodeling in chronic disease may be permanent
unknown etiology, there have been associations with amphetamine diet aids, contaminated rapeseed oil, and contaminated l-tryptophan.
Patients present with substernal chest pain or pressure, exertional dyspnea, fatigue, and possibly syncope.
Chest x-ray will show prominent pulmonary arterial vasculature
ECG will may show right ventricular hypertrophy
High resolution CT, Perfusion nuclear scanning, MRI, and angiography may all be useful. Cardiac cath may be needed as well. Lung biopsy may be a final, necessary step to make a diagnosis of cause for PH.
PaO2<55 or PaO2<59 with Crit>55, p pulmonale, or edema should be treated with chronic supplemental O2
CCBs, Iv nitroglycerin, IV Prostacyclin, epoprostenol (Flolan), eventual lung transplantation
vasodilator therapy is not without risks as it can cause systemic hypotension or worsen PH b/c if the pulmonary diameter is fixed, it will just cause decreased RH pressures without affecting pulmonary.
at risk for venous thromboembolic disease
chronic VTE can also be the cause of pulmonary hypertension and often the patient will have dramatic improvement if the clot is removed
Estimation of Mean Pulmonary Artery Pressure
(Chest. 2008; 133:592-593)
An invasive study by our team1 has challenged this model by reporting that sPAP accounts for 98% of mPAP variability in resting humans studied over à range of 10 to 78 mm Hg, and that a new formula (mPAP = 0.61 sPAP + 2) reasonably predicts mPAP, with a 0 ± 2 mm Hg bias (mean ± SD). Our retrospective analysis1 of the pressure data previously published by Laskey et al2 led to similar conclusion. The principle that underlies scientific modeling cautions against favoring the complex models over the simple ones,3 and this favors the use of sPAP only to estimate mPAP, without the need to include dPAP in the model. Although initially challenged,4 our findings have been confirmed in children free of congenital heart diseases,5 and have proved useful to estimate mPAP in large-scale studies performed in both adults6 and children7 for whom only Doppler-derived sPAP data are available. Finally, a linear relationship between mPAP and sPAP has also been documented in pulmonary arterial hypertension patients performing graded, submaximal supine exercise both before and after a 6-week prostacyclin treatment.8
can cause pulmonary hypertension
PAH associated with syncope, vasovagal, and sudden death
hypoxemia and hypercarbia are both vasoconstrictors
sleep apnea to pulm htn to apnea to worsening pulm htn
coumadin o2 diuretics
Hanging Flolan using normal IV pump
1. Get Intervia (empty IV bag) and light proof plastic bag.
2. Mix Flolan with sterile diluent
3. Inject Flolan into intervia
4. Place Ice on both sides in light-proof bag
5. Use normal IV tubing, no filter required.
6. Convert pts 24 hour rate to hourly rate
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