Cardiovascular Disease |

Pulmonary Hypertension and Cardiovascular Complications in Patients With Ventilator Associated Pneumonia FREE TO VIEW

Bhuvin Buddhdev, MD; Mary Naglak, PhD; Michael Shoemaker, PhD; Rajkumar Dasgupta, MD
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Abington Memorial Hospital, Abington, PA

Chest. 2013;144(4_MeetingAbstracts):165A. doi:10.1378/chest.1703218
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SESSION TITLE: Cardiovascular Posters

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 30, 2013 at 01:30 PM - 02:30 PM

PURPOSE: To determine prevalence of pulmonary hypertension (PH) and cardiovascular conditions in patients with ventilator associated pneumonia (VAP) and its influence on new onset or worsening of pre-existing PH or cardiovascular complications.

METHODS: Retrospective medical record analysis of intensive care unit patients with VAP. Records were reviewed for clinical characteristics, including sociodemographic data, echocardiogram, electrocardiogram, cardiac biomarkers and serum creatinine 60 days before and after developing VAP. Statistical analysis included descriptive statistics and chi square analysis to compare clinical characteristics between those with and without PH.

RESULTS: Eight-six records were reviewed, including 51 (59%) males and 35 (41%) females. Mean age was 64.6±18 years. Before VAP 68% had an abnormal electrocardiogram due to rhythm disturbance (21%), ischemic heart disease (10%), or both (37%). Following development of VAP, 30% of patients developed new electrocardiographic changes to include rhythm disturbance (19%), ischemic heart disease (9%), or both (2%). Laboratory data before VAP included elevated cardiac β natriuretic peptide (BNP) (70%), cardiac troponins (50%), serum creatinine (37%), and creatinine phosphokinase-MB (32%). The greatest biomarker change after VAP was cardiac BNP (worse in 44% patients), followed by cardiac troponins (26%), serum creatinine (16%), and creatinine phosphokinase-MB (8%). Available echocardiogram results suggested that 52% had PH before developing VAP and 62% had new onset or worsening of PH after VAP. There were no differences in clinical characteristics between those with and without PH (p>.05). New onset or worsening of PH after VAP was not associated with worsening left ventricular dysfunction (p>.05).

CONCLUSIONS: Pulmonary hypertension and underlying cardiac conditions are major risk factors for the development of VAP. New onset or worsening of PH is a complication of VAP secondary to hypoxia and is independent of left ventricular dysfunction. Additionally, there is increased risk of cardiovascular complications within 60 days following VAP.

CLINICAL IMPLICATIONS: The present study demonstrates the need for laboratory testing of cardiac biomarkers, electrocardiogram and echocardiogram in patients with VAP. Role of pulmonary vasodilators to treat PH secondary to VAP warrants further investigation.

DISCLOSURE: The following authors have nothing to disclose: Bhuvin Buddhdev, Mary Naglak, Michael Shoemaker, Rajkumar Dasgupta

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