Jon-Emile S. Kenny MD [@heart_lung] “… when you walk around a kitchen, you will say to yourself, this is interesting, this is grand, this is beautiful like Chardin.” -Marcel Proust Background Titration of positive end-expiratory pressure [PEEP] in the acute respiratory distress syndrome [ARDS] is achieved by a diverse assortment of practices undergirded by equally [… read more]
Jon-Emile S. Kenny MD [@heart_lung] “It’s these expressions, I never give, That keep me searching for a heart of gold … And I’m gettin’ old.” -Neil Young An 86 year old woman is admitted with progressive dyspnea and lower extremity edema. 8 months ago she received a trans-catheter aortic valve replacement (TAVR) for severe aortic [… read more]
Jon-Emile S. Kenny MD [@heart_lung] With the birth of ‘fluid responsiveness’ physiology [1], there has been a slow and solemn drumbeat ushering the central venous pressure [CVP] up the squeaking planks of the hemodynamic gallows [2, 3]. Despite this, a few years ago I made a humble defense of the central venous pressure. Importantly, I was [… read more]
Jon-Emile S. Kenny MD [@heart_lung] “Upward, not northward.” -E. A. Abbott A pressure chamber within a pressure chamber; the heart within the thorax. These are two pumps beating in-and-out of time, varying in physiology and pathophysiology between patients and within any one patient during the arc of an illness. As such, when we inspect the [… read more]
Jon-Emile S. Kenny MD [@heart_lung] with illustrations by Carla M. Canepa MD Pilots of high-performance, tactical fighter jets each have continuous positive airway pressure [i.e. CPAP] masks as a part of their flight suit. Strikingly, beyond the clinically-commonplace airway pressure of 5-15 cm of H2O, a fighter pilot may endure a mask-applied pressure of 90 [… read more]
By Jon-Emile S. Kenny [@heart_lung] When interpreting hemodynamic studies of drugs which – potentially – alter the resistance of the pulmonary vascular tree, we often turn to the calculated pulmonary vascular resistance [cPVR] as our guide. For instance, a vasopressor determined to increase the cPVR is wholly avoided in a patient with pulmonary arterial hypertension. We [… read more]
By Jon-Emile S. Kenny [@heart_lung] “The only way to get rid of temptation is to yield to it.” -Oscar Wilde The Case A 76 year old woman without known medical comorbidity is ambulating along 7th avenue, rounding the corner where St. Vincent’s Hospital once operated. It is an exceptionally humid August afternoon and she has not [… read more]
Jon-Emile S. Kenny [@heart_lung] While parts 1 and 2 of this trilogy considered the mechanical power applied to the lung skeleton and the effects of lung inhomogeneity [i.e. ‘stress raisers’], respectively; this final installment will draw the reader towards the pulmonary vasculature as a key mediator of ventilator induced lung injury [VILI]. That the pulmonary [… read more]
Jon-Emile S. Kenny [@heart_lung] In part 2, I continue my commentary on this excellent review; part 1 may be found here. In this post I will consider patients with severe metabolic acidosis and those with right ventricular [RV] dysfunction and/or failure. Severe Metabolic Acidosis In patients with severe metabolic acidosis, alveolar ventilation tends to be maximal [… read more]
ICU Physiology in 1000 Words The Right Ventricular Afterload [Part 2 of 2] Jon-Emile S. Kenny M.D. [@heart_lung] Having considered the short-comings of Laplace’s Law and the PVR with respect to the RV afterload in part 1, we will now turn to each of the following in turn: the pulmonary arterial input impedance, a measureable [… read more]
By Parth Rali, MD and Marvin Balaan, MD Submassive pulmonary emboli (PE) are those that are severe enough to produce right ventricular dysfunction on echocardiogram or elevated biomarkers (mainly troponin), but not hemodynamic instability (i.e., systemic blood pressure and cardiac output are preserved). The management of the patient with submassive PE is a matter of controversy with several [… read more]
Image: EKOS Patients with acute pulmonary embolism (PE) fall into three general clinical categories: Massive PE, most often defined as hypotension due to right ventricular dysfunction. Short-term mortality is high (more than 1 in 7 die in-hospital). Systemic thrombolytic therapy (tissue plasminogen activator or tPA) is considered standard care by AHA and ACCP, because it [… read more]
Choosing Wisely, the initiative for medical cost-effectiveness (don’t call it rationing!) of the American Board of Internal Medicine, included the use of vasodilators for pulmonary hypertension owing to left heart disease or hypoxemic lung disease (WHO Groups II and III) as #2 on its top five “no-no’s” in its new pulmonology section. The “Five Things Physicians and [… read more]
A large phase III randomized trial testing Ambrisentan (Letairis) for early idiopathic pulmonary fibrosis was stopped early after an interim analysis of the data showed possible harm. The results were reported in Annals of Internal Medicine. Patients being treated with Letairis had more evidence of progression of idiopathic pulmonary fibrosis and were hospitalized more often, including [… read more]
New Pulmonary Hypertension Drug Riociguat Proves Effective Pulmonary arterial hypertension is a rare but life-threatening illness affecting around 10,000 people in the U.S., in which ongoing remodeling of the pulmonary vasculature leads to narrowed pulmonary arteries with increased pulmonary artery pressure (pulmonary hypertension), and if untreated, eventual right heart failure and death. (The overwhelming majority [… read more]
Pulmonary Hypertension 2013 Update/Review Part 2 of 2: Treatment of PH Read Part 1: Diagnosis and Classification of Pulmonary Hypertension by Brett Ley, MD There are 3 classes of pulmonary vasodilator drugs: phosphodiesterase-5 inhibitors (PDE-5 inhibitors, e.g. sildenafil, tadalafil), endothelin receptor antagonists (ERAs, e.g. bosentan, ambrisentan), and prostacyclins (epoprostenol, iloprost, treprostinil). Because the large trials [… read more]
Pulmonary Hypertension Update/Review Part 1 of 2: Classification and Diagnosis Read Part 2: Treatment of PAH by Brett Ley, MD Pulmonary hypertension (PH) is defined simply as a mean pulmonary artery pressure of 25 mmHg or greater. However, this entity encompasses a heterogeneous group of patients and underlying etiologies where accurate diagnosis, correct physiologic classification, and careful evaluation for [… read more]
In Most Patients with Pulmonary Embolism, Central Clot is Worse than Peripheral by Brett Ley, MD Pulmonary embolism (PE) presents with a wide range of clinical severity and course. Management decisions (level of care, length of observation, and aggressive therapies such as thrombolysis) are generally based on a patient’s risk of a poor outcome. Guidelines recommend risk [… read more]
Xarelto (rivaroxaban): New FDA Indication for DVT, PE The U.S. Food and Drug Administration (FDA) approved Bayer’s Xarelto (rivaroxaban) for a new indication for treating deep vein thrombosis (DVT) or pulmonary embolism (PE), and for long-term prophylaxis of recurrent DVT and PE. Xarelto already had FDA approval for prevention of DVTs and PEs after knee or [… read more]
Idiopathic Pulmonary Fibrosis (IPF) 2012 Review (More PulmCCM Topic Updates) This document is updated periodically as new research findings in IPF are published. What Causes IPF? (Etiology/Pathogenesis of IPF) Since it’s still called “idiopathic,” you probably figured out already that the cause(s) of IPF remain unknown. Researchers use a paradigm for studying idiopathic pulmonary fibrosis called [… read more]
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