Distributive, Vasodilatory, Neurogenic, and Septic
1. A 76-year-old woman with a history of ischemic cardiomyopathy with known severely decreased left ventricular (LV) systolic function presents with 1 day of nausea, vomiting, right flank pain, fevers, and chills. In the emergency room she is confused. Her temperature is 39 °C, BP is 80/60 mm Hg, HR is 110 bpm, respiratory rate (RR) is 22 breaths/min, and her arterial oxygen saturation is 99% by pulse oximetry while breathing room air. Her physical examination is significant for clear lungs and warm, well-perfused extremities. Initial laboratory studies were significant for blood white cell count (WBC) of 18 × 109/L with 90% neutrophils, lactate of 3 mmol/L, and creatinine of 1.4 mg/dL. Urinalysis was significant for 50 WBC per high-power field (HPF). The patient is started on ceftriaxone for pyelonephritis and resuscitated with 3 L of intravenous (IV) normal saline. Four hours later, the patient’s BP is 90/64 mm Hg, HR is 106 bpm, RR is 24 breaths/min, and arterial oxygen saturation is 99% by pulse oximetry while breathing room air. She is now obtunded. She does not appear to be in respiratory distress, and her extremities remain warm and well-perfused and lungs are still clear to auscultation. Her serum lactate is now 3.8 mmol/L. Bedside ultrasound images are shown in Figures 42.1, 42.2, and 42.3 ( Videos 42.1, 42.2, and 42.3).
Which of the following statements is most accurate?
A. The patient is in cardiogenic shock.
B. The patient is likely to tolerate additional IV fluids.
C. It is impossible for a patient like this to have high stroke volume (SV) and cardiac output (CO).
D. None of the above.
1. Correct Answer: B. The patient is likely to tolerate additional IV fluids.
Rationale: This patient with premorbid cardiomyopathy and decreased LV systolic function presents with septic shock secondary to pyelonephritis. After initial fluid resuscitation, her BP remains low, with signs of organ hypoperfusion. The presence of A-line pattern on lung ultrasound suggests that left atrial pressure (LAP) is not elevated. Correlation between IVC static and dynamic parameters is imperfect and is affected by extraneous factors, such as intra-abdominal pressure, spontaneous (vs. mechanical) ventilation, inspiratory effort, and premorbid fitness. Nonetheless, a very small IVC that is completely collapsing on inspiration suggests that right atrial pressure (RAP) is not elevated.
Utility of using static and/or dynamic IVC parameters to predict volume responsiveness in shock is disputed. Nonetheless, normal/low LAP and RAP suggest that this patient is likely to be fluid tolerant. The concept of fluid tolerance, as opposed to fluid responsiveness, is central to understanding of shock management. Fluid responsiveness is the increase in 10% to 15% of CO when you give a 500 cc bolus of fluids or do passive leg raise. Fluid intolerance is when IV fluids are no longer helpful and may cause harm. In patients with sepsis and vasodilation, even if they are persistently hypotensive and tachycardic, at some point, fluids will no longer increase the CO because the flat portion of the Starling curve is reached and continuing to give fluids has been shown to increase mortality.
1. Dipti A, Soucy Z, Surana A, Chandra S. Role of inferior vena cava diameter in assessment of volume status: a meta-analysis. Am J Emerg Med. 2012;30(8):1414-1419.
2. Jankowich M, Gartman E. Ultrasound in the Intensive Care Unit. Humana Press, Springer; 2015.
3. Lichtenstein DA, Mezière GA, Lagoueyte JF, Biderman P, Goldstein I, Gepner A. Lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009; 136:10141-1020.
4. Orso D, Paoli I, Piani T, Cilenti FL, Cristiani L, Guglielmo N. Accuracy of ultrasonographic measurements of inferior vena cava to determine fluid responsiveness: a systematic review and meta-analysis. J Intensive Care Med. 2020;35(4):354-363.
2. An 86-year-old man is transferred from a nursing home with fever, cough, and hypoxemia. On presentation, his temperature is 39 °C, BP is 90/60 mm Hg, HR is 112 bpm, RR is 36 breaths/min, arterial oxygen saturation is 90% on 100% non-rebreather mask. His physical examination is notable for crackles in the right middle and lower lung fields. Laboratory studies show a blood WBC of 32 × 109/L, lactate of 2.4 mmol/L, and creatinine of 1.2 mg/dL. Admission chest X-ray shows right middle and right lower lobe consolidations. The patient is intubated for hypoxic respiratory failure secondary to multifocal pneumonia, given 4 L IV fluids, and started on vancomycin and piperacillin/tazobactam. The next hospital day, the patient’s BP is 92/66 mm Hg and his HR is 110 bpm. Bedside ultrasound images are shown in Figures 42.4, 42.5, 42.6A, 42.6B, and 42.7 ( Videos 42.4, 42.5, 42.6A, 42.6B, and 42.7).
Figure 42.6 A. Right lower lung field. Coronal plane, posterior axillary line. B. Lung ultrasound. Anterior chest wall bilaterally.
Which of the following statements is most accurate?
A. The patient is in pulmonary edema and should not be given additional IV fluids.
B. Given unreliability of the inferior vena cava (IVC) parameters in ventilated patients, invasive monitoring is needed for estimation of intracardiac pressures and volume status.
C. The patient is likely fluid responsive.
D. Positive pressure ventilation (PPV) is expected to decrease IVC size and increase its collapsibility.
2. Correct Answer: C. The patient is likely fluid responsive.
Rationale: In spontaneously breathing patients air enters the lungs because of negative intrathoracic pressure generated during inspiration. This same negative intrathoracic pressure sucks blood from the abdominal IVC into the thorax and the right atrium (RA), causing decrease in IVC size on inspiration. In patients on PPV air instead is forced into the lungs by an external device and, if the patient is “passive on the ventilator,” increases intrathoracic pressure on inspiration. This increase in intrathoracic pressure is transmitted to the RA and causes decrease in blood return from the IVC. Consequently, PPV reverses the relationship between the phases of respiratory cycle and IVC size, with decrease in IVC occurring during expiration instead of inspiration. In addition, essentially all PPV includes positive end-expiratory pressure (PEEP), which means that at its lowest (during expiration) intrathoracic pressure is still higher than in spontaneously breathing persons (in whom end-expiratory pressure is zero). This elevation of intrathoracic pressure tends to increase IVC size (a static parameter) and to alter the relationship between RAP and IVC size.
Multiple studies have failed to consistently identify a single cutoff of static and/or dynamic IVC parameters in distinguishing patients with shock who are fluid responsive from those who are not. Despite that, if one allows for a “gray zone” that is diagnostically noninformative, studies support the use of IVC size at its extremes. A very small IVC in a patient who is passive on a ventilator strongly suggests low RAP. Even though RAP is not synonymous with fluid responsiveness, it is often a useful marker when more sophisticated methods are not available.
In addition, in this patient lung ultrasound A-pattern suggests that the patient is not in pulmonary edema and can likely tolerate additional IV fluids, that is, is likely to be fluid tolerant.
1. Jankowich M, Gartman E. Ultrasound in the Intensive Care Unit. Human Press; 2015.
2. Via G, Tavazzi G, Price S. Ten situations where inferior vena cava ultrasound may fail to accurately predict fluid responsiveness: a physiologic based point of view. Intensive Care Med. 2016;42:1164-1167.
3. Viellard-Baron A, Evrard B, Repesse X, et al. Limited value of end-expiratory inferior vena cava diameter to predict fluid responsiveness impact of intra-abdominal pressure. Intensive Care Med. 2018;44:197-203.
3. A 72-year-old man with renal cell carcinoma presents with neutropenic fever and is found to have left lower lobe pneumonia. He is started on broad-spectrum antibiotics and given 3 L of IV fluids. He remains hypotensive with BP of 80/60 mm Hg, HR of 120 bpm, RR of 24 breaths/min, and arterial oxygen saturation of 94% by pulse oximetry on 4 L of oxygen via nasal cannula. His lactate is 1.2 mmol/L, and creatinine is 1.0 mg/dL. Bedside ultrasound is performed and shown in Figures 42.8A, 42.8B, 42.9, and 42.10 ( Videos 42.8A, 42.8B, 42.9, and 42.10).
Figure 42.8 A. Left lower lung. Coronal plane, posterior axillary line. B. Lung ultrasound. Left anterior chest wall.