Thread by @Sam_Brusca

Tweetorial of heart-lung interactions in the setting of mechanical ventilation (MCV) from @cardionerds episode 20. cardionerds.com/episodes/covid…

These concepts will apply to critically ill COVID-19 patients that are developing concurrent respiratory and cardiac failure.

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In patients with significant respiratory distress and concurrent LV dysfunction, intubation and MCV can stabilize hemodynamics. Significant increased work of breathing is associated with large pleural pressure swings, which increase both LV and RV afterload.

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Negative pleural pressures increase LV afterload by increasing transmural pressure (TMp) and wall tension (like a vacuum sucking the LV, preventing contraction).

Here, the LV must generate 110mmHg in order to maintain flow to the extrathoracic aorta and TMp = 120mmHg.

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After intubation, patients with hypoxia and LV failure often benefit from higher PEEP strategies. In this scenario, the PEEP both recruits lung to improve compliance and oxygenation and augments LV performance by decreasing LV TMp (like a hand squeezing the LV).

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PEEP is also transmitted to the RA, which can decrease venous return and optimize an LV that has fallen off the Starling curve.

Careful/slow PEEP titration is imperative, as it is difficult to predict at what level RV stroke volume will be adversely affected.

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Further, higher levels of PEEP and large tidal volumes can unmask RV dysfunction, which was previously not identified. This is due to increased transpulmonary pressure (TPp; Palveolar - Ppleural) and lung volume, which determine pulmonary vascular resistance (PVR).

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In pts with primary RV dysfunction or cor pulmonale 2/2 hypoxia, MCV is complicated.

Some PEEP can optimize RV-LV interdependence and improve LV compliance and stroke volume by reducing RVEDV.

Too much PEEP, however, will increase PVR and induce progressive RV failure.

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When preparing a patient with significant LV dysfunction for extubation, it is prudent to perform a T-piece trial. This allows you to observe for hemodynamic collapse when the patient is removed from positive pleural pressures and exposed to negative pleural pressures.

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Hemodynamic effects of MCV are dependent on the balance of lung and chest wall compliance. Chest wall < lung compliance leads to higher pleural pressures and increased venous return and LV afterload effects. In contrast, TPp increases are blunted and PVR is less affected.

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Interpretation of intravenous pressures (e.g. from a Swan) should account for respiratory system compliance. The pressures will be appreciably affected by positive pressures in the setting of obesity and may be minimally affected by positive pressures in ARDS.

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How helpful was this for understanding heart-lung interactions during MCV?