Note, this video is compressed from a lecture I recently gave in Montreal at 'The Hospitalist & the Resuscitationist' conference.
Intended Learning Outcomes
Predict the change in the portal vein Doppler waveform as a patient is placed into prone position
Relate the hemodynamic effects of prone position to inhaled pulmonary vasodilators
Predict how prone position may affect a patient with left ventricular systolic dysfunction
Explain the physiology of right ventricular outflow tract obstruction with prone position
Understand pulse pressure variation between supine and prone positions in ARDS
Part A [complete alone] ----------------
The patient from module 8 has worsening respiratory status in the emergency department and he is sedated, pharmacologically paralyzed and intubated. He had an extremely anterior airway and despite using a bougie on first attempt, multiple airway endeavours were required. Following the second attempt, he had large gastric acid aspiration. His saturations fell dramatically and he was placed on PEEP of 15 cm H2O with low tidal volume ventilation. Despite an FiO2 of 1.0, his PaO2 was only 70 mmHg and his lactate rose.
T or F: on ultrasound his IVC will be fixed and dilated?
T or F: there will be pulse pressure variation in his arterial line?
T or F: the pulsatility of his portal vein will shrink?
The ICU fellow arrives and he is concerned about the rising lactate & ARDS. He looks at the patient’s IVC using a pocket ultrasound. He discusses the case with the senior ED fellow; she describes to him why further fluid loading was ceased given the clinical gestalt and pulsatile portal vein. Further, they look at his lungs and note bilateral anterior B-lines and a severely impaired left ventricle with moderate to severe mitral regurgitation. The fellow agrees with the senior resident’s assessment and no further crystalloids are given. The patient is brought to the ICU and 3 hours later the patient's gas exchange and pulmonary mechanics worsen. The patient is then placed in prone position and, shortly thereafter, started on inhaled epoprostenol.
T or F: with pronation and inhaled vasodilators this patient’s portal vein pulsatility will fall?
T or F: with pronation and inhaled vasodilators, this patient’s pulse pressure variation will diminish?
Roughly 20 minutes following initiation of inhaled epoprostenol, the patient’s hemodynamics and oxygenation acutely worsen. He remains paralyzed, and his plateau pressure has increased significantly.
T or F: the patient likely has right ventricular outflow tract obstruction from a shrunken right ventricle?
T or F: urgent volume removal with dialysis will worsen his outflow tract obstruction and hemodynamics?
Reflect on learning modules 4 and 7 and 8; what is your understanding of pulse pressure variation, its mechanism and relationship to volume status and volume responsiveness? How does prone position affect right ventricular hemodynamics and central venous pressure? How might this be different depending on a patient’s overall volume status and left ventricular function? Is your inclination to give the patient in this case fluids or dialysis? How does your pre-test probability affect your interpretation of his ultrasound results?
Part B [complete alone] ----------------
1. Watch this video
Learning Module Nine
Part C [complete together] ----------------
1. Return to the combined Rahn-Guyton diagram that you drew in module 7; explain to each other how the left ventricle and volume status may affect this diagram – think in terms of RV preload and afterload.
2. Return to the case from module 4; how is that patient’s physiology different from the case in this module? Recall your cartoon of the fearless red blood cell sailing through the venous system in this patient. Imagine a red blood cell sailing through the module 4 patient’s venous system from supine to prone. Do the same for the patient in case above. Each partner should select one patient and explain to each other your reasoning.
3. Hypothesize how prone position and inhaled pulmonary vasodilators will independently affect portal vein pulsatility; think in terms of the Guyton Diagram. Further, think about why portal vein assessment is particularly useful in prone patients.
4. Can you imagine a scenario when prone position and inhaled pulmonary vasodilators may make portal vein pulsatility increase? How might you predict this before starting these therapies? Again, use the combined Rahn-Guyton Diagram as an explanatory tool; always consider changes in pleural pressure, preload and afterload.
5. Reconsider the case from part A. and the true or false questions. What do you think was the cause of the decompensation in the ICU? What further information might you want to know? How might starting epinephrine affect the patient above? What would epinephrine do to this patient’s portal vein pulse and arterial pulse pressure variation? What about priming a dialysis unit with 250 mL of venous blood? How would that affect portal vein and arterial pulse? Think in terms of RV preload and afterload.
6. With your learning partner, explain to each other the risk factors for right ventricular outflow tract obstruction and if you think it played a role in this case; how might portal vein pulse look in a patient with RVOT obstruction upon pronation?
7. Find another learning team and review the intended learning outcomes. Did everyone meet them? Discuss 2 unanswered questions that you still have following the module; how might you answer these questions?
The first 4 chapters will cover basic physiology and pathophysiology with an emphasis on the Campbell and Guyton Diagrams.
The remaining 4 chapters will focus on clinically-relevant topics in the intensive care unit; the discussions will be largely drawn from the physiology covered in the first half of the textbook.
Heart-lung.org will provide a comprehensive, on-line tutorial in cardiovascular and respiratory physiology for the interested medical student, resident and fellow.