Intended Learning Outcomes
Explain why the calculated pulmonary vascular resistance can rise when there is recruitment and dilation of the pulmonary vascular tree.
Use the pulmonary arterial diastolic pressure – pulmonary artery occlusion pressure difference to explain how prone position [or any hemodynamic intervention] affects the pulmonary arterial tree
Hypothesize how prone position can challenge a poorly functioning left heart
Understand the ‘index of transmission’ and its application in the ICU
Part A [complete alone] ----------------
The patient from modules 8 & 9 was returned to the supine position and inhaled epoprostenol was stopped following his worsening gas exchange. Your current ICU attending trained in the era of pulmonary artery flotation catheters. She decides to place one to get a better sense of the patient’s hemodynamics. While the patient is supine, sedated and paralyzed, his initial numbers are as follows - all pressures are end-expiratory:
Pulmonary Artery Systolic Pressure: 60 mmHg
Pulmonary Artery Diastolic Pressure: 40 mmHg
Pulmonary artery occlusion pressure 30 mmHg
Cardiac output: 3.7 L/min
PEEP is 20 cm H2O and Plateau pressure is 33 cm H2O; from end-expiration to end-inspiration, the pulmonary artery occlusion pressure increases from 30 mmHg to 32 mmHg.
T or F: the pulmonary vascular resistance is high?
T or F: both prone position and inhaled vasodilators should be re-initiated?
T or F: Prone position will raise the pulmonary artery occlusion pressure?
T or F: The Index of Transmission is less than 10%
The attending then decides to place the patient back in prone, without starting inhaled epoprostenol. When settled in prone position, the attending is meticulous about re-leveling the pressure transducer to exactly the level of the right atrium – presumed to be 5 cm above the level of the bed/sternum. The patient’s hemodynamics are obtained again after 30 minutes in prone when his gas exchange worsens again.
Pulmonary Artery Systolic Pressure: 73 mmHg
Pulmonary Artery Diastolic Pressure: 44 mmHg
End-expiratory pulmonary artery occlusion pressure 40 mmHg
Cardiac output: 3.0 L/min
PEEP is 20 cm H2O and Plateau pressure is 33 cm H2O; from end-expiration to end-inspiration, the pulmonary artery occlusion pressure now increases from 40 mmHg to 44 mmHg.
T or F: when placed in prone position, the patient’s right ventricular afterload was unchanged?
T or F: when in prone position, the chest wall to total respiratory system stiffness increased?
T or F: when placed in prone position, the pulmonary artery pulse pressure increased?
T or F: the index of transmission remained unchanged?
What is your understanding of pulmonary vascular resistance? What do you think happens to the pulmonary arterial resistance to flow in ARDS when a patient is placed into the prone position? Was this confirmed in the numbers above? What is your understanding of how the airway pressure on the ventilator affects the pleural and vascular pressure within the thorax? Is there a way to correct for this?
Part B [complete alone] ----------------
1. Watch this video
This video is a portion of the lecture from chapter 7D
Learning Module Ten
2. Read this brief essay on the pulmonary vascular resistance & the 'Thoughts & Clinical Implications' section from a post on the SIOVAC Trial found here
Part C [complete together] ----------------
1. One member of the learning team calculate the pulmonary vascular resistance in Wood Units for the patient in supine, the other calculate pulmonary vascular resistance for the patient in prone. What values do you obtain? Explain to each other the implications for this patient.
2. One learning partner should explain to the other why the pulmonary arterial pulse pressure rose, but overall cardiac output fell. How is this somewhat paradoxical? What are some possible reasons? How might trans-esophageal echocardiography help test your hypothesis?
3. The learner in exercise 2 should now become the teacher and explain the meaning of the pulmonary arterial diastolic pressure – pulmonary arterial occlusion pressure difference. How did this change from supine to prone?
4. Come to a conclusion about the right ventricular afterload in this patient and draw a Guyton Diagram for the right ventricle for this patient in the supine and prone positions; then do the same for the left ventricular cardiac function curve.
5. Reconsider the true or false questions from the case as a learning team. Do you think that VV-ECMO would help this patient’s hemodynamics? Why or why not? What about a balloon pump? Why or why not? What do you think dobutamine would do? Try to use the Guyton Diagram as an explanatory model. Focus on the left ventricular cardiac function curve and the pulmonary venous return curve.
6. With your learning partner, explain to each other the meaning of the index of transmission. Why does this change on prone position? Hypothetically if, instead of prone position, an inhaled vasodilator was initiated which had exactly the same hemodynamic response as prone position, but the patient remained in the supine position. What would the patient’s estimated absolute pressures be?
7. Find another learning team and review each of the intended learning outcomes. Act like you are all on rounds in the ICU. How would you transmit these outcomes to the team on rounds? Someone be the attending and run rounds with the goal of meeting all of the intended learning outcomes.
8. Bonus question: read this article and hypothesize how the patient’s right ventricular ejection pressure changed from supine to prone position.
Heart-lung.org will provide a comprehensive, on-line tutorial in cardiovascular and respiratory physiology for the interested medical student, resident and fellow.
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.