Objective: To review treatment and outcomes of septic shock in patients with pulmonary hypertension (PH) managed at a tertiary care institution.Design, setting and patients: We identified consecutive patients with non-cardiac PH (non-Group 2 in the World Health Organization classification) who were treated for septic shock in four intensive care units at a tertiary care institution between July 2004 and July 2007. Patients with a left ventricular ejection fraction <50%, diastolic dysfunction, pericardial effusion or significant valve disease were excluded. Descriptive statistics were used to analyse the data.Main outcome measures: Hospital mortality, duration of vasopressor and ventilatory support, length of hospital and ICU stay.Results: The final group for analysis comprised 82 patients; The major causes of PH were chronic obstructive pulmonary disease, interstitial lung disease and portopulmonary hypertension. PH was mild in 46 patients (56%), moderate in 21(26%) and severe in 15 (18%). Vasopressor treatment was initiated in 69 patients (84%) within the first 48 hours: noradrenaline was most commonly used (53 patients, 65%), and 51 patients (62%) were treated with more than one agent. Sixty-seven patients (82%) were mechanically ventilated, and 33 (40%) required renal replacement therapy. Forty-three patients (52%) survived to hospital discharge; 23 (28%) remained alive at 1 year. Hospital mortality increased with severity of PH: 28% in mild, 67% in moderate and 80% in severe PH. Non-survivors were more likely to have plateau pressures beyond 30 cm H2O while mechanically ventilated within the first 48 hours in the ICU (56% v 29%, P=0.03), to develop atrial fibrillation (AF) (46% v 12%, P < 0.001), and to require longer vasopressor support (mean, 5.3 v 2.6 days, P=0.003). In a multivariate logistic regression analysis, severity of PH (odds ratio [OR], 1.55; 95% CI, 1.04-2.46; P=0.04), new-onset AF (OR, 6.51; 95% CI, 2.24-22.07; P < 0.001) and longer duration of vasopressor support (OR, 1.15; 95% CI, 1.03-1.34; P=0.04) were associated with increased hospital mortality.Conclusions: The severity of PH, new-onset AF, and longer vasopressor support were associated with poor outcomes in patients with PH who developed severe sepsis and septic shock.

Pulmonary artery pressure elevation complicates the course of many complex disorders treated in a noncardiac intensive care unit. Acute pulmonary hypertension, however, remains underdiagnosed and its treatment frequently begins only after serious complications have developed. Significant pathophysiologic differences between acute and chronic pulmonary hypertension make current classification and treatment recommendations for chronic pulmonary hypertension barely applicable to acute pulmonary hypertension. In order to clarify the terminology of acute pulmonary hypertension and distinguish it from chronic pulmonary hypertension, we provide a classifi cation of acute pulmonary hypertension according to underlying pathophysiologic mechanisms, clinical features, natural history, and response to treatment. Based on available data, therapy of acute arterial pulmonary hypertension should generally be aimed at acutely relieving right ventricular (RV) pressure overload and preventing RV dysfunction. Cases of severe acute pulmonary hypertension complicated by RV failure and systemic arterial hypotension are real clinical challenges requiring tight hemodynamic monitoring and aggressive treatment including combinations of pulmonary vasodilators, inotropic agents and systemic arterial vasoconstrictors. The choice of vasopressor and inotropes in patients with acute pulmonary hypertension should take into consideration their effects on vascular resistance and cardiac output when used alone or in combinations with other agents, and must be individualized based on patient response.